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Research Progress on Anti-aging Active Ingredients of Soybean
WUHailing, SUNMengyan, SUOHaicui, RENHailong, ZHANGWenting, SUNMingyang, SHENYingbin, YUANQinghua
Chin Agric Sci Bull ›› 2026, Vol. 42 ›› Issue (8) : 198-210.
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Abbreviation (ISO4): Chin Agric Sci Bull
Editor in chief: Yulong YIN
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Research Progress on Anti-aging Active Ingredients of Soybean
To gain an in-depth understanding of the research progress of soybean active ingredients, reveal their roles in anti-aging mechanisms, and promote the in-depth development and application of soybean active ingredients as natural anti-aging products, this paper systematically reviews the relevant research progress of soybean active ingredients in aging models. The physicochemical properties and basic efficacy of main active ingredients of soybeans are summarized, including soybean peptides, soybean isoflavones, soybean saponins, and soybean phospholipids. It analyzes the mechanisms by which soybean active ingredients regulate aging based on the three major theories: free radical damage, inflammatory senescence, and immunosenescence. It is concluded that soybean active ingredients can not only exert a core anti-aging effect by scavenging free radicals, inhibiting inflammatory responses, and regulating immune responses, but also achieve systemic regulation of organismal aging by ameliorating the functional decline of the nervous and endocrine systems, delaying skeletal and skin aging, and maintaining intracellular homeostasis, and ultimately exert their anti-aging effects. In summary, this paper proposes that: (1) most existing studies on the physicochemical properties of soybean active ingredients are limited to static characterization and do not fully consider the dynamic physiological processes and microenvironmental effects in vivo. Therefore, future research should employ dynamic tracking technologies that simulate in vivo processes to elucidate the changes in characteristics of soybean active ingredients during digestion, absorption, and blood transportation, thereby providing more realistic scientific evidence for mechanistic studies. (2) The anti-aging effect of soybean active ingredients exhibits multi-target regulatory characteristics, yet the interaction patterns among multiple anti-aging mechanisms mediated by individual components have not been systematically elucidated. This restricts the in-depth understanding of their essential mechanism of action and the efficient development of functional products. Therefore, future research should integrate multi-omics technologies and focus on the regulatory networks of individual components in anti-aging pathways, so as to provide mechanistic support for precisely unlocking their anti-aging potential and promoting targeted product development. (3) Current studies mainly rely on induced aging models, which cannot fully simulate the chronic process and complex microenvironment of natural human aging. Future research should optimize the model system to better match the characteristics of natural human aging, thereby providing more reliable scientific evidence for the clinical translation of soybean anti-aging products.
soybean / active ingredients / soybean isoflavones / soybean peptides / anti-aging / antioxidant / anti-inflammatory
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The aging process is one of the best examples of the effects of a deterioration of homeostasis, since aging is accompanied by an impairment of the physiological systems including the homeostatic systems such as the immune system. We propose an integrative theory of aging providing answers to the how (oxidation), where first (mitochondria of differentiated cells) and why (pleiotropic genes) this process occurs. In agreement with this oxidation-mitochondrial theory of aging, we have observed that the age-related changes of immune functions have as their basis an oxidative and inflammatory stress situation, which has among its intracellular mechanisms the activation of NFkappaB in immune cells. Moreover, we have also observed that several functions of immune cells are good markers of biological age and predictors of longevity. Based on the above we have proposed the theory of oxidation-inflammation as the main cause of aging. Accordingly, the chronic oxidative stress that appears with age affects all cells and especially those of the regulatory systems, such as the nervous, endocrine and immune systems and the communication between them. This fact prevents an adequate homeostasis and, therefore, the preservation of health. We have also proposed a key involvement of the immune system in the aging process of the organism, concretely in the rate of aging, since there is a relation between the redox state and functional capacity of the immune cells and the longevity of individuals. Moreover, the role of the immune system in senescence could be of universal application. A confirmation of the central role of the immune system in oxi-inflamm-aging is that the administration of adequate amounts of antioxidants in the diet, improves the immune functions, decreasing their oxidative stress, and consequently increases the longevity of the subjects.
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陈俊斌. 大豆皂苷A1经调控TLR4/MyD88信号通路降低炎症状态下肝脏胆固醇的作用与机理研究[D]. 广州: 南方医科大学, 2023.
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In the present study, we assessed the extraction of low molecular weight soluble polysaccharides (MESP) from soybean by-products using microwave-assisted enzymatic technology and proposed the chemical structure of MESP using Fourier transform-infrared spectroscopy, gas chromatography, and 1H and 13C nuclear magnetic resonance spectrum analysis. The results suggested that MESP mainly comprised arabinose, rhamnose, and glucuronic acid with (1→4) glycosidic linkages in the backbone. Compared with inulin, MESP was found to selectively stimulate the growth of Lactobacillus probiotics. Moreover, the results of in vitro fermentation indicated that MESP significantly increased the concentrations of both acetate and butyrate (p < 0.05). MESP were treated on lipopolysaccharide (LPS)-stimulated RAW264.7 cells to determine the anti-inflammatory effect in vitro. It was observed that MESP inhibited nitric oxide, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 production. Furthermore, Western blotting results indicated that MESP significantly attenuated LPS-induced downregulation of phosphorylation levels of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) in macrophages. The underlying mechanism might involve inhibition of the expression of pro-inflammatory cytokines, presumably via JAK2/STAT3 pathway. Collectively, the results of our study paved way for the production of MESP, which may be potentially used as nutraceutical ingredients for prebiotics and anti-inflammatory agents, from soybean residue.
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Inflammation contributes to various diseases and soybeans and legumes are shown to reduce inflammation. However, the bioactive ingredients involved and mechanisms are not completely known. We hypothesized that soy isoflavones daidzin and daidzein exhibit anti-inflammatory effect in lipopolysaccharides (LPS)-stimulated RAW264.7 macrophage cell model and that activation mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways may mediate the effect.Cell viability and nitric oxide (NO) level were determined by 3-(4,5)-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Griess reagent respectively. ELISA kits and Western blotting respectively assessed the generations of pro-inflammatory cytokines and protein expressions of signaling molecules. p65 nuclear translocation was determined by immunofluorescence assay.The in vitro results showed that both isoflavones did not affect cell viability at the concentrations being tested and significantly reduced levels of NO, pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), and inflammatory indicators such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in RAW264.7 cells. Daidzin and daidzein partially suppressed MAPK signaling pathways, reducing the phosphorylation of p38 and ERK; whilst phosphorylation of JNK was mildly but not significantly decreased. For the involvement of NF-κB signaling pathways, daidzin only reduced the phosphorylation of p65 whereas daidzein effectively inhibited the phosphorylation of IKKα/β, IκBα and p65. Daidzin and daidzein inhibited p65 nuclear translocation, comparable with dexamethasone (positive control).This study supports the anti-inflammatory effects of isoflavones daidzin and daidzein, which were at least partially mediated through inactivation of MAPK and/or NF-κB signaling pathways in macrophages.© 2022. The Author(s).
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Cytokines and chemokines are transcriptionally regulated by inflammatory transcription factors such as nuclear factor-κB (NF-κB), activator protein-1 (AP-1), and interferon regulatory factor (IRF)-3. A daidzein derivative compound, 8-hydroxydaidzein (8-HD), isolated from soy products, has recently gained attention due to various pharmacological benefits, including anti-inflammatory activities. However, regulation of the inflammatory signaling mechanism for 8-HD is still poorly understood, particularly with respect to the IRF-3 signaling pathway. In this study, we explored the molecular mechanism of 8-HD in regulating inflammatory processes, with a focus on the IRF-3 signaling pathway using a lipopolysaccharide (LPS) and polyinosinic:polycytidylic acid [Poly (I:C)] stimulated murine macrophage cell line (RAW264.7). The 8-HD downregulated the mRNA expression level of IRF-3-dependent genes by inhibiting phosphorylation of the IRF-3 transcription factor. The inhibitory mechanism of 8-HD in the IRF-3 signaling pathway was shown to inhibit the kinase activity of IKKε to phosphorylate IRF-3. This compound can also interfere with the TRIF-mediated complex formation composed of TRAF3, TANK, and IKKε leading to downregulation of AKT phosphorylation and reduction of IRF-3 activation, resulted in inhibition of IRF-3-dependent expression of genes including IFN-β, C-X-C motif chemokine 10 (CXCL10), and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). Therefore, these results strongly suggest that 8-HD can act as a promising compound with the regulatory function of IRF-3-mediated inflammatory responses.
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吉雅, 胡玉萍, 张海龙, 等. 大豆短肽颗粒剂抗衰老和免疫调节作用研究[J]. 内蒙古中医药, 2014, 33(7):95-96.
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李硕. 大豆小分子肽对机体保健功能作用的研究[D]. 昆明: 昆明理工大学, 2013.
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戴汉慧, 田庆伟, 王永明, 等. 大豆异黄酮对衰老模型小鼠免疫功能的影响[J]. 中国食品添加剂, 2003(5):50-53.
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顾饶胜, 范红艳, 王艳春, 等. 大豆异黄酮对D-半乳糖所致衰老大鼠的影响[J]. 吉林医药学院学报, 2013, 34(3):161-164.
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Considerable efforts have been made to understand the role of oxidative stress in age-related diseases and ageing. The mitochondrial free radical theory of ageing, which proposes that damage to mitochondrial DNA (mtDNA) and other macromolecules caused by the production of reactive oxygen species (ROS) during cellular respiration drives ageing, has for a long time been the central hypothesis in the field. However, in contrast with this theory, evidence from an increasing number of experimental studies has suggested that mtDNA mutations may be generated by replication errors rather than by accumulated oxidative damage. Furthermore, interventions to modulate ROS levels in humans and animal models have not produced consistent results in terms of delaying disease progression and extending lifespan. A number of recent experimental findings strongly question the mitochondrial free radical theory of ageing, leading to the emergence of new theories of how age-associated mitochondrial dysfunction may lead to ageing. These new hypotheses are mainly based on the underlying notion that, despite their deleterious role, ROS are essential signalling molecules that mediate stress responses in general and the stress response to age-dependent damage in particular. This novel view of ROS roles has a clear impact on the interpretation of studies in which antioxidants have been used to treat human age-related diseases commonly linked to oxidative stress.© 2013 The Association for the Publication of the Journal of Internal Medicine.
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杨同攀. 大豆皂苷对D-半乳糖诱导衰老小鼠肾脏抗氧化作用的影响[D]. 延吉: 延边大学, 2016.
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张月. 大豆皂苷对D-半乳糖所致小鼠衰老的延缓作用及其机制研究[D]. 延吉: 延边大学, 2015.
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Substantial increases in the relative and absolute number of older persons in our society pose a challenge for biology, social and behavioral science, and medicine. Successful aging is multidimensional, encompassing the avoidance of disease and disability, the maintenance of high physical and cognitive function, and sustained engagement in social and productive activities. Research has identified factors predictive of success in these critical domains. The stage is set for intervention studies to enhance the proportion of our population aging successfully.
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This short review goes back to early discoveries concerning the neuroendocrinology of aging, discussing the Brown-Sequard experiment on rejuvenation at the end of the 19th century and Steinach's subsequent experiments in the early 20th century. It also considers the seminal experiments of Pierre Ascheim, Ming Tsung Peng and Joseph Meites in the 1960s on the aging of the gonadotrophic axis. Major age-associated changes in neuroendocrine regulatory processes involved in the menopausal transition, andropause, somatopause and adrenopause are also reviewed. Finally, some views on future directions of research into the neuroendocrinology of aging are proposed, based on the pleiotropy of neuroendocrine messengers and functions.
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Studies on animals have shown that chronic stress is able to evoke behavioral changes such as locomotor activity deficit, decreased sleep, reduced food and water consumption and impaired memory. Chronic stress produces changes in concentrations of neurotransmitters, mainly in the hippocampus. The hippocampus is a vulnerable brain structure that is involved in learning and memory functions. In this study, we investigated the effects of chronic stress procedure and moclobemide in rats, and the influence of chronic stress on the levels of monoamines: noradrenaline (NE), dopamine (DA) and serotonin (5-HT) in the rat hippocampus [as well as their metabolites: dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA)]. It was found out that chronic 21-day stress caused worsening of memory: the well trained rats after stress procedure lost their ability to find food quickly. Because of many errors in finding the way, the time these animals needed was on average 2.4-times longer than that of the control group. Single, as well as prolonged (21 days) treatment with moclobemide (10 mg/kg/day) counteracted the deficit of memory induced by chronic stress. In stressed animals, we observed an increase in DA, decrease in DOPAC, 5-HT and 5-HIAA and decrease in NE levels. Moclobemide modulated the changes in the levels of neurotransmitters in the hippocampus, decreasing their turnover. The results demonstrate that moclobemide improves memory impaired by stress. They suggest also that moclobemide has a modulatory effect on stress-induced neurotransmitter changes which may be of importance for the protective effect of the drug with regard to memory impairment.
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谢丽平. 具有抗氧化、抗衰老活性的多肽筛选、分离纯化及结构鉴定[D]. 广州: 华南理工大学, 2019.
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SAMP8 mice have a shorter lifespan and show the dysfunction of the central nervous system. We here investigated whether soy peptides (SP) composed mainly of di- and tripeptides has the potential to prevent age-dependent cognitive impairment. SAMP8 and normal aging mice, SAMR1, were fed a diet supplemented with SP or a control diet for 26 weeks to investigate the preventive effects on the progression of cognitive decline using the Morris water maze. The SP-fed groups in SAMP8 and SAMR1 prevented the decline of cognitive ability compared to their controls. Increased expression of neurotrophic factors such as BDNF and NT-3 at mRNA and protein levels were observed in the brain of SP-fed mice, especially SAMP8. Further, the phosphorylated CREB protein level of SAMP8 was markedly up-regulated by SP feeding. These suggest that SPs have the potential for prevention of cognitive impairment via neurotrophic effects.
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顾饶胜, 王艳春, 刘微, 等. 大豆异黄酮对急性衰老小鼠学习记忆障碍的改善作用[J]. 吉林医药学院学报, 2007, 28(3):125-127.
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张禄平, 杨倩, 张玉森, 等. 白藜芦醇联合大豆异黄酮对衰老模型大鼠学习记忆能力及葡萄糖转运蛋白表达的影响[J]. 卫生研究, 2020, 49(2):249-253.
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杜丽根, 阮云军, 王玉筵, 等. 大豆异黄酮延缓脐静脉内皮细胞衰老的机制研究[J]. 广州医科大学学报, 2018, 46(6):25-28.
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朱建林, 杨桂莲, 黄忆明. 大豆异黄酮对去卵巢小鼠认知功能的影响[J]. 中南大学学报(医学版), 2004, 29(1):81-83.
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买文丽, 刘红, 许薇, 等. 大豆异黄酮对去卵巢大鼠空间记忆和海马单胺类递质影响[J]. 辽宁中医药大学学报, 2014, 16(1):35-37.
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Apoptosis is a vital component in the evolutionarily conserved host defense system. Apoptosis is the guardian of tissue integrity by removing unfit and injured cells without evoking inflammation. However, apoptosis seems to be a double-edged sword since during low-level chronic stress, such as in aging, increased resistance to apoptosis can lead to the survival of functionally deficient, post-mitotic cells with damaged housekeeping functions. Senescent cells are remarkably resistant to apoptosis, and several studies indicate that host defense mechanisms can enhance anti-apoptotic signaling, which subsequently induces a senescent, pro-inflammatory phenotype during the aging process. At the molecular level, age-related resistance to apoptosis involves (1) functional deficiency in p53 network, (2) increased activity in the NF-κB-IAP/JNK axis, and (3) changes in molecular chaperones, microRNAs, and epigenetic regulation. We will discuss the molecular basis of age-related resistance to apoptosis and emphasize that increased resistance could enhance the aging process.
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In replicative senescence, cells undergo permanent exit from cell cycle traverse; this is traditionally thought to occur at the end of a culture's in vitro life span, after serial passaging. In general, the checkpoint for replicative senescence is found at the G(1)/S border, controlled by the modulation of a battery of proteins, typified by gaining inhibitors of cell cycle traverse, such as cyclin-dependent kinases or RB hyperphosphorylation, and losing pro-proliferation gene expressions such as c-fos, c-myc, and a cadre of proliferation-dependent kinases. Here, we present evidence that replicatively senescent fibroblasts are resistant to apoptotic death, associated with a lack of key enzyme activities, caspase-3 being the chief executioner. This observation, coupled with our earlier report that senescent fibroblasts maintain persistently high levels of pro-survival factor Bcl-2, suggests that the molecular signaling program present in fibroblasts at the end of their in vitro life span may not only cater to the state of permanent exit from cell cycle traverse, but also dictate an inability to commit cellular suicide. Future experiments will reveal whether replicatively senescent fibroblasts that can neither proliferate nor die contribute to organismic aging, and whether their accumulation over time in tissue becomes detrimental to the normal aging process.
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温海霞, 赵薇, 刘国艺, 等. 大豆异黄酮对初老大鼠卵巢Bcl-2基因和Caspase-3基因mRNA表达的影响[J]. 沈阳药科大学学报, 2007, 24(11):710-714,720.
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Ovarian aging is characterized by declines in follicular reserve and oocyte quality due, in part, to increased oxidative stress and apoptosis. Soy isoflavones (ISOs) have been shown to improve ovarian lifespan by acting as antioxidant and antiapoptotic agents. We aimed at evaluating whether ISOs could modulate oxidative stress and reduce apoptosis and improve ovarian follicle survival in middle-aged female rats. Twelve ovary-intact female Wistar rats (12-month-old) were divided into groups: control (CTRL) and ISO, daily treated by gavage with vehicle or soy-ISO extract (150 mg/kg b.w), respectively. After 8 weeks, rats were euthanized and their ovaries removed for histomorphometric (% follicles) and apoptosis (cleaved-caspase-3/BCL2 immunostaining) evaluations, or subjected to biochemical assays to survey reactive oxygen species (ROS) and lipid peroxidation levels and total antioxidant capacity (TAC). The frequency of atretic follicles and number of cleaved-caspase-3-positive cells, as well as the ROS and lipid peroxidation levels, were significantly lower in ISO group compared to CTRL. A significantly higher number of BCL2-positive cells and TAC levels were also observed in ISO group. In conclusion, soy ISOs could decrease follicular atresia, apoptosis and oxidative stress, as well as increase the TAC in ovaries of female rats.
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郑元林, 杨敏, 毛缜, 等. 大豆黄酮在D-半乳糖致衰老小鼠肝组织氧化损伤中的保护作用[J]. 徐州师范大学学报(自然科学版), 2008, 26(4):1-7.
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Genistein, a soy isoflavone, exhibits a biphasic effect on cells proliferation with some different effects between ER-alpha and ER-beta. The objective of this present study is to determine the modulatory effect based on cell cycle progression under genistein treatment in combination with 17-β estradiol (E2) on CHO-K1 cells. The effect of genistein 0.1-100 µM on cells proliferation was examined by MTT assay. The modulation of genistein and estradiol (E2) on cell cycle and apoptosis were observed by using flowcytometry with PI and PI/AnnexinV staining, respectively. Moreover, the effect of genistein and E2 on senescence cells, and ROS level were determined by senescence-associated β-galactosidase (SA β-gal) staining and by using flowcytometry with 2', 7'-dichlorofluorescin diacetate (DCFDA) staining, respectively. The expression level of the cell cycle and senescence protein markers were observed by immunoblotting. Single treatment of genistein at physiologically achievable (low) concentration (<2 µM) induced proliferation of CHO-K1 cells while at a pharmacological (high) concentration (50 and 100 µM) suppressed cells proliferation. Interestingly, treatment of genistein at the physiological concentration in combination with E2 for 24, 48 and 72 h decreased cells viability on CHO-K1 cells compared to untreated cells. Further analysis of the cells showed that 50 µM genistein induced G2/M phase accumulation and induced apoptosis. Moreover, genistein induced cell senescence and increased ROS level. Immunoblotting analysis showed the decreasing of ERalpha, Bcl2, and ppRb protein level upon treatment of 1 µM Gen and 1 nM E2. Our results suggest that the cell proliferation inhibitory mechanism of genistein at pharmacological concentration involved the induction of cell senescence, and the elevation of ROS level. Moreover, the decreased of cells proliferation upon treatment of physiological concentration of genistein in combination with E2 may be correlated with the alteration of ER expression.© 2019 The Author (s).
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孙玲, 魏振承, 徐志宏, 等. 大豆异黄酮对衰老小鼠羟脯氨酸等物质变化的影响[J]. 中国粮油学报, 2003, 18(2):58-60.
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翁宇静. 大豆苷元对皮肤胶原合成的影响及机理初探[D]. 上海: 华东师范大学, 2010.
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Soy isoflavone is an attractive source of functional cosmetic materials with anti-wrinkle, whitening and skin hydration effects. After consumption, the majority of soy isoflavones are converted to their metabolites in the human gastrointestinal tract. To understand the physiological impact of soy isoflavone on the human body, it is necessary to evaluate and address the biological function of its metabolites. In this study, we investigated the effect of 6,7,4'-trihydroxyisoflavone (6,7,4'-THIF), a major metabolite of daidzein, against solar UV (sUV)-induced matrix metalloproteinases (MMPs) in normal human dermal fibroblasts. MMPs play a critical role in the degradation of collagen in skin, thereby accelerating the aging process of skin. The mitogen-activated protein/extracellular signal-regulated kinase (MEK)/extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MKK)3/6/p38 and MKK4/c-Jun N-terminal kinases (JNK) signaling pathways are known to modulate MMP-1 function, and their activation by sUV was significantly reduced by 6,7,4'-THIF pretreatment. Our results also indicated that the enzyme activity of protein kinase C (PKC)α, an upstream regulator of MKKs signaling, is suppressed by 6,7,4'-THIF using the in vitro kinase assay. Furthermore, the direct interaction between 6,7,4'-THIF and endogenous PKCα was confirmed using the pull-down assay. Not only sUV-induced MMP-1 expression, but also sUV-induced signaling pathway activation were decreased in PKCα knockdown cells. Overall, we elucidated the inhibitory effect of 6,7,4'-THIF on sUV-induced MMPs and suggest PKCα as its direct molecular target.
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Ovariectomy accelerates age-related skin changes as adequate oestrogen levels are required to control structural integrity and functional capacity of skin. Genistein, a soy-derived isoflavone, has been tested in anti-ageing cosmetic preparations with interesting results on skin elasticity, photoaging and skin cancer prevention. We investigated the effects of genistein aglycone and compared them with systemic raloxifene hydrochloride and 17-α-ethinyloestradiol on skin changes in aged, ovariectomized (OVX) rats.Six months after ovariectomy, rats were randomly allocated to different groups and treated, daily, with genistein aglycone (1 and 10mg·kg(-1) s.c.), raloxifene hydrochloride (0.05 and 0.5mg·kg(-1) s.c.) or 17-α-ethinyloestradiol (0.003 and 0.03mg·kg(-1) s.c.) for 12 weeks. Controls were untreated OVX and sham OVX rats. At the end of the treatment period, a skin biopsy was carried out and skin samples were assessed for molecular, histological and functional changes.Skin samples of untreated OVX rats showed a decrease in TGF-β1, VEGF, MMP-2, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 compared with sham OVX rats. All the treatments significantly restored this depressed molecular profile revealed in OVX rats. Genistein aglycone, 1mg·kg(-1), also significantly increased the thickness of collagen and breaking strength of skin in the OVX rats.Relatively long-term, systemic treatment with genistein aglycone shows comparable efficacy to oestrogen in reversing some molecular, histological and functional changes of the skin associated with ovariectomy in aged rats. This suggests that genistein aglycone might be an effective alternative therapy for the management of age-related skin changes in postmenopausal women.© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
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靳莉, 高学敏, 汪锦邦, 等. 大豆总皂苷抗衰老作用的研究Ⅱ.抗衰老功能的实验研究[J]. 食品工业科技, 1999(S1):39-41.
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巩菊芳, 邵邻相. 大豆磷脂对小鼠皮肤胶原蛋白含量的影响[J]. 中国生化药物杂志, 2003, 24(6):292-293.
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谌萌. 基于秀丽隐杆线虫模型研究大豆肽对年龄相关肌肉退变的作用[D]. 无锡: 江南大学, 2022.
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刘丰彬, 马炳存, 赵斌. 6周负重跑训练和补充大豆多肽对D-半乳糖衰老大鼠骨骼肌IGF-ImRNA和GDF-8mRNA表达的影响[J]. 中国运动医学杂志, 2010, 29(6):673-676,692.
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Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration.
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Patients with end-stage liver disease exhibit progressive skeletal muscle atrophy, highlighting a negative crosstalk between the injured liver and muscle. Our study was to determine whether TGFβ ligands function as the mediators. Acute or chronic liver injury was induced by a single or repeated administration of carbon tetrachloride. Skeletal muscle injury and repair was induced by intramuscular injection of cardiotoxin. Activin type IIB receptor (ActRIIB) ligands and growth differentiation factor 8 (Gdf8) were neutralized with ActRIIB-Fc fusion protein and a Gdf8-specific antibody, respectively. We found that acute hepatic injury induced rapid and adverse responses in muscle, which was blunted by neutralizing ActRIIB ligands. Chronic liver injury caused muscle atrophy and repair defects, which were prevented or reversed by inactivating ActRIIB ligands. Furthermore, we found that pericentral hepatocytes produce excessive Gdf8 in injured mouse liver and cirrhotic human liver. Specific inactivation of Gdf8 prevented liver injury-induced muscle atrophy, similar to neutralization of ActRIIB ligands. Inhibition of Gdf8 also reversed muscle atrophy in a treatment paradigm following chronic liver injury. Direct injection of exogenous Gdf8 protein into muscle along with acute focal muscle injury recapitulated similar dysregulated muscle regeneration as that observed with liver injury. The results indicate that injured liver negatively communicate with the muscle largely via Gdf8. Unexpectedly, inactivation of Gdf8 simultaneously ameliorated liver fibrosis in mice following chronic liver injury. In vitro, Gdf8 induced human hepatic stellate (LX-2) cells to form a septa-like structure and stimulated expression of profibrotic factors. Our findings identified Gdf8 as a novel hepatomyokine contributing to injured liver–muscle negative crosstalk along with liver injury progression.
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陈成. 大豆蛋白活性肽保健功能性的研究[J]. 大豆通报, 2005(2):22-24.
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张聪慧. 大豆异黄酮代谢产物对秀丽隐杆线虫的抗衰老作用及其机制研究[D]. 保定: 河北农业大学, 2014.
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