FASEB JOURNAL
·
2026
·Vol. 40
·期 19
·e72336
·
IF 4.3
Zengfeng Guo,Ningfeng Zhang,Junshen Huang,Wang Zhang,Yawei Hu,Shaochu Chen,Ming Gong,Jianhua Zhou,Jiancheng Yang,Jiawen Wu
Postmenopausal osteoporosis (PMOP) is frequently complicated by iron accumulation, which exacerbates bone loss. Baicalein, a natural flavonoid with iron-chelating and antioxidant properties, has shown bone-protective effects, but its role in iron-overloaded PMOP remains unclear. This study investigated whether baicalein ameliorates iron-accumulated PMOP by inhibiting osteoclastogenesis via Nrf2 activation. In vitro, bone marrow-derived macrophages (BMMs) were induced into osteoclasts with RANKL under iron overload. Baicalein (10 μM) suppressed osteoclast differentiation, F-actin ring formation, and bone resorption, reduced intracellular and mitochondrial ROS, lowered Fe 2+ and total iron content, and upregulated Nrf2 nuclear translocation and HO-1 expression. These effects were abrogated by the Nrf2 inhibitor ML385 or Nrf2 siRNA. In vivo, an ovariectomized (OVX) mouse model with iron dextran injection (100 mg/kg/week) was used. Oral baicalein treatment (100 mg/kg/day) significantly prevented bone loss, improved bone microarchitecture and biomechanical properties, reduced iron deposition in bone, liver and spleen, lowered serum ferritin and bone ROS, and activated Nrf2 signaling in bone tissue. Co-administration of ML385 reversed these protective effects. Collectively, baicalein ameliorates iron-accumulated postmenopausal osteoporosis by activating the Nrf2 pathway, thereby inhibiting osteoclast differentiation and bone resorption. Baicalein represents a promising multi-target candidate for treating PMOP, especially in patients with concomitant iron accumulation. Graphical Baicalein inhibits osteoclastogenesis in vitro and attenuates iron accumulation-associated postmenopausal osteoporosis in vivo. Mechanistically, baicalein targetedly activates Nrf2, subsequently leading to the activation of antioxidant enzymes, which facilitates the elimination of intracellular ROS. The reduced ROS levels attenuate RANKL-induced NFATc1 expression, thereby suppressing the transcription of osteoclast-related genes and ultimately inhibiting osteoclastogenesis.
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JOURNAL OF APPLIED TOXICOLOGY
·
2023
·
IF 3.3
Miao Xing,Xiaoyu Ma,Xi Wang,Haoze Wang,Minjuan Xie,Ziwen Zhang,Jie Zhou
Emodin has been demonstrated to possess multiple pharmacological activities. However, emodin has also been reported to induce nephrotoxicity at high doses and with long-term use, and the underlying mechanism has not been fully disclosed. The current study aimed to investigate the roles of oxidative stress and ferroptosis in emodin-induced kidney toxicity. Mice were intraperitoneally treated with emodin, and NRK-52E cells were exposed to emodin in the presence or absence of treatment with Jagged1, SC79, or t-BHQ. Emodin significantly upregulated the levels of blood urea nitrogen, serum creatinine, malondialdehyde, and Fe 2+ , reduced the levels of superoxide dismutase and glutathione, and induced pathological changes in the kidneys in vivo. Moreover, the viability of NRK-52E cells treated with emodin was reduced, and emodin induced iron accumulation, excessive reactive oxygen species production, and lipid peroxidation and depolarized the mitochondrial membrane potential ( ΔΨm ). In addition, emodin treatment downregulated the activity of neurogenic locus notch homolog protein 1 (Notch1), reduced the nuclear translocation of nuclear factor erythroid-2 related factor 2 (Nrf2), and decreased glutathione peroxidase 4 protein levels. However, Notch1 activation by Jagged1 pretreatment, Akt activation by SC79 pretreatment, or Nrf2 activation by t-BHQ pretreatment attenuated the toxic effects of emodin in NRK-52E cells. Taken together, these results revealed that emodin-induced ferroptosis triggered kidney toxicity through inhibition of the Notch1/Nrf2/glutathione peroxidase 4 axis.
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Genes
·
2023
·Vol. 14
·期 5
·1011
·
IF 3.5
Lei Yang,Sheng He,Ling Ling,Fangfang Wang,Lei Xu,Lei Fang,Fan Wu,Shuting Zhou,Fan Yang,Hongwei Wei,Duonan Yu
miR-144/451and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) regulate two antioxidative systems that have been identified to maintain redox homeostasis in erythroid cells by removing excess reactive oxygen species (ROS). Whether these two genes coordinate to affect ROS scavenging and the anemic phenotype, or which gene is more important for recovery from acute anemia, has not been explored. To address these questions, we crossedmiR-144/451knockout (KO) andNrf2KO mice and examined the phenotype change in the animals as well as the ROS levels in erythroid cells either at baseline or under stress condition. Several discoveries were made in this study. First,Nrf2/miR-144/451double-KO mice unexpectedly exhibit similar anemic phenotypes asmiR-144/451single-KO mice during stable erythropoiesis, although compound mutations ofmiR-144/451andNrf2lead to higher ROS levels in erythrocytes than single gene mutations. Second,Nrf2/miR-144/451double-mutant mice exhibit more dramatic reticulocytosis thanmiR-144/451orNrf2single-KO mice during days 3 to 7 after inducing acute hemolytic anemia using phenylhydrazine (PHZ), indicating a synergistic effect ofmiR-144/451and Nrf2 on PHZ-induced stress erythropoiesis. However, the coordination does not persist during the whole recovery stage of PHZ-induced anemia; instead,Nrf2/miR-144/451double-KO mice follow a recovery pattern similar tomiR-144/451single-KO mice during the remaining period of erythropoiesis. Third, the complete recovery from PHZ-induced acute anemia inmiR-144/451KO mice takes longer than inNrf2KO mice. Our findings demonstrate that complicated crosstalk betweenmiR-144/451and Nrf2 does exist and the crosstalk of these two antioxidant systems is development-stage-dependent. Our findings also demonstrate thatmiRNAdeficiency could result in a more profound defect of erythropoiesis than dysfunctional transcription factors.Keywords:miR-144/451;Nrf2;hemolytic anemia;reactive oxygen species
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JOURNAL OF ETHNOPHARMACOLOGY
·
2023
·
IF 5.4
Xiaoju Zhuge,Xiaosheng Jin,Tingting Ji,Rongzhou Li,Liwei Xue,Weilai Yu,Zijiao Quan,Haibin Tong,Fang Xu
Ethnopharmacological relevance The dried fruit of Gardenia jasminoides Ellis (Zhizi in Chinese) is a traditional medicine used for thousands of years in China, Japan and Korea. Zhizi was recorded in Shennong Herbal , as a folk medicine, it reduces fever and treats gastrointestinal disturbance with antiphlogistic effects. Geniposide , an iridoid glycoside , is an important bioactive compound derived from Zhizi and possesses remarkable antioxidant and anti-inflammatory capacities. The pharmacological efficacy of Zhizi is highly related to the antioxidant and anti-inflammatory effects of geniposide. Aim of the study Ulcerative colitis (UC) is a common chronic gastrointestinal disease as a global public health threat. Redox imbalance is an essential factor in the progression and recurrence of UC. This study aimed to explore the therapeutic effect of geniposide on colitis and uncover the underlying mechanisms of geniposide-mediated antioxidant and anti-inflammatory activities. Experimental design The study design involved investigating the novel mechanism by which geniposide ameliorates dextran sulfate sodium (DSS)-induced colitis in vivo and lipopolysaccharide (LPS)-challenged colonic epithelial cells in vitro . Materials and methods The protective effect of geniposide against colitis was evaluated by histopathologic observation and biochemical analysis of colonic tissues in DSS-induced colitis mice. The antioxidant and anti-inflammatory effects of geniposide were evaluated in both DSS-induced colitis mice and LPS-challenged colonic epithelial cells. Immunoprecipitation , drug affinity responsive target stability (DARTS), and molecular docking were performed to identify the potential therapeutic target of geniposide and the potential binding sites and patterns. Results Geniposide ameliorated the symptoms of DSS-induced colitis and colonic barrier injury, inhibited pro-inflammatory cytokine expression, and suppressed activation of the NF-κB signaling in colonic tissues of DSS-challenged mice. Geniposide also ameliorated lipid peroxidation and restored redox homeostasis in DSS-treated colonic tissues. In addition, in vitro experiments also showed that geniposide exhibited significant anti-inflammatory and antioxidant activity , as evidenced by suppressed IκB-α and p65 phosphorylation and IκB-α degradation, and enhanced the phosphorylation and transcriptional activity of Nrf2 in LPS-treated Caco2 cells. ML385, a specific Nrf2 inhibitor, abolished the protective effect of geniposide against LPS-induced inflammation. Mechanistically, geniposide could bind to KEAP1 , thereby disrupting the interaction between KEAP1 and Nrf2, preventing Nrf2 from degradation and activating the Nrf2/ARE signaling pathway, ultimately suppressing the onset of inflammation caused by redox imbalance. Conclusions Geniposide ameliorates colitis by activation of Nrf2/ARE signaling, while preventing colonic redox imbalance and inflammatory damage, indicating that geniposide can be considered as a promising lead compound for the treatment of colitis.
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PHYTOMEDICINE
·
2023
·
IF 7.9
Yong Fang Gong,Shu Hou,Jia-Cheng Xu,Yan Chen,Le-Le Zhu,Ying-Ying Xu,Yu-Qing Chen,Miao-Miao Li,Li-Li Li,Jing-Jing Yang,Yan Yang
Background Phosphorylated Smad3 isoforms are reversible and antagonistic, and the tumour-suppressive pSmad3C can shift to an oncogenic pSmad3L signal. In addition, Nrf2 has a two-way regulatory effect on tumours, protecting normal cells from carcinogens and promoting tumour cell survival in chemotherapeutics. Accordingly, we hypothesised that the transformation of pSmad3C/3L is the basis for Nrf2 to produce both pro- and/or anti-tumourigenic effects in hepatocarcinogenesis . Astragaloside IV (AS-IV), the major component of Astragalus membranaceus , exerts anti-fibrogenic and carcinogenic actions. Lately, AS-IV administration could delay the occurrence of primary liver cancer by persistently inhibiting the fibrogenesis and regulating pSmad3C/3 L and Nrf2/HO-1 pathways synchronously. However, effect of AS-IV on hepatocarcinogenesis implicated in the bidirectional cross-talking of pSmad3C/3 L and Nrf2/HO-1 signalling, especially which one contributes palpably than the other still remains unclear. Purpose This study aims to settle the above questions by using in vivo (pSmad3C +/− and Nrf2 −/− mice) and in vitro (plasmid- or lentivirus- transfected HepG2 cells) models of HCC . Study design and methods The correlation of Nrf2 to pSmad3C/pSmad3L in HepG2 cells was analysed by Co-immunoprecipitation and dual-luciferase reporter assay. Pathological changes of Nrf2, pSmad3C, and pSmad3L in human HCC patients, pSmad3C +/- mice, and Nrf2 −/- mice were gauged by immunohistochemical, haematoxylin and eosin staining, Masson, and immunofluorescence assays. Finally, western blot and qPCR were used to verify the bidirectional cross-talking of pSmad3C/3L and Nrf2/HO-1 signalling protein and mRNA in vivo and in vitro models of HCC. Results Histopathological manifestations and biochemical indicators revealed that pSmad3C +/- could abate the ameliorative effects of AS-IV on fibrogenic/carcinogenic mice with Nrf2/HO-1 deactivation and pSmad3C/p21 transform to pSmad3L/PAI-1//c-Myc. As expected, cell experiments confirmed that upregulating pSmad3C boosts the inhibitory activity of AS-IV on phenotypes (cell proliferation, migration and invasion), followed by a shift of pSmad3L to pSmad3C and activation of Nrf2/HO-1. Synchronously, experiments in Nrf2 −/- mice and lentivirus-carried Nrf2shRNA cell echoed the results of pSmad3C knockdown. Complementarily, Nrf2 overexpression resulted in the opposite result. Furthermore, Nrf2/HO-1 contributes to AS-IV's anti-HCC effect palpably compared with pSmad3C/3L. Conclusion These studies highlight that harnessing the bidirectional crosstalk pSmad3C/3 L and Nrf2/HO-1, especially Nrf2/HO-1 signalling, acts more effectively in AS-IV's anti-hepatocarcinogenesis, which may provide an important theoretical foundation for the use of AS-IV against HCC.
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FOLIA HISTOCHEMICA ET CYTOBIOLOGICA
·
2023
·Vol. 61
·期 2
·109-122
·
IF 1.5
Jiahui Han Di Jia Hao Yao Ting Lv Xi Xu Xin Ge
Introduction. Hemorrhagic shock (HS) is an important cause of high mortality in traumatized patients. Cryptotanshinone (CTS) is a bioactive compound extracted from Salvia miltiorrhiza Bunge (Danshen). The current study aimed to explore the effect and underlying mechanism of CTS on the liver injury induced by HS. Material and methods. Male Sprague-Dawley rats were used to establish the HS model by hemorrhaging and monitoring mean arterial pressure (MAP). CTS was intravenously administered at concentration of 3.5 mg/kg, 7 mg/kg, or 14 mg/kg 30 minutes before resuscitation. Twenty-four hours after resuscitation, the liver tissue and serum samples were collected for the following examinations. Hematoxylin and eosin (H&E) staining was used to evaluate hepatic morphology changes. The myeloperoxidase (MPO) activity in liver tissue and the serum activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were examined to reveal the extent of liver injury. The protein expression of Bax and Bcl-2 in liver tissue was detected by western blot. The TUNEL assay determined the apoptosis of hepatocytes. Oxidative stress of liver tissue was assessed by the examination of reactive oxygen species (ROS) generation. The content of malondialdehyde (MDA), glutathione (GSH), and adenosine triphosphate (ATP), the activity of superoxide dismutase (SOD) and oxidative chain complexes (complex I, II, III, IV), as well as cytochrome c expression in cytoplasm and mitochondria, were also used to determine the extent of oxidative injury in the liver. Immunofluorescence (IF) was employed to estimate nuclear factor E2-related factor 2 (Nrf2) expression. The mRNA and protein levels of heme oxygenase 1 (HO-1), NAD(P)H: quinone oxidoreductases 1 (NQO1), cyclooxygenase-2 (COX-2), and nitric oxide synthase (iNOS) were assessed by real-time qPCR, western blot to investigate the mechanism of CTS regulating HS-induced liver injury. Results. H&E staining and a histological score of rat liver suggested that HS induced liver injury. The activity of ALT, AST, and MPO was significantly increased by HS treatment. After CTS administration the ALT, AST, and MPO activities were suppressed, which indicates the liver injury was alleviated by CTS. The HS-induced upregulation of the TUNEL-positive cell rate was suppressed by various doses of CTS. HS-induced ROS production was decreased and the protein expression of Bax and Bcl-2 in the HS-induced rat liver was reversed by CTS administration. In the liver of HS-induced rats, the upregulation of MDA content and the downregulation of GSH content and SOD activity were suppressed by CTS. Additionally, CTS increases ATP content and mitochondrial oxidative complexes activities and suppressed the release of cytochrome c from mitochondria to the cytoplasm. Moreover, IF and western blot demonstrated that the activation of Nrf2 blocked by HS was recovered by different doses of CTS in liver tissue. The expression of downstream enzymes of the Nrf2 pathway, including HO-1, NQO1, COX-2, and iNOS, was reversed by CTS in the HS rat model. Conclusions. The current study for the first time revealed the protective effect of CTS in HS-induced liver injury. CTS effectively recovered hepatocyte apoptosis, oxidative stress, and mitochondria damage induced by HS in the rat liver partly via regulating the Nrf2 signaling pathway.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2022
·
IF 5.895
Jiaxin Li,Hengju Ge,Yang Xu,Jiahong Xie,Fujie Yan,Wei Chen
Geniposide (GEN), a main compound extracted from Gardenia jasminoides fruit, has various biological activities including anti-inflammation, cellular damage alleviation, neuroprotection, and others. However, the effect of GEN on oxidative stress in hepatic cells is yet to be investigated. Our study uncovered that GEN eliminated excess intracellular free radicals by activating the Nrf2/ARE signaling pathway in H2O2-treated hepatocytes, while the protective effect was blocked by ML385 (an inhibitor of Nrf2). Moreover, H2O2 led to upregulation of miR-27b-3p in L02 cells, which was restrained by GEN. Overexpression of miR-27b-3p greatly weakened the antioxidant capacity of GEN in hepatocytes via directly targeting the Nrf2 gene. Our findings indicated that GEN treatment recovered H2O2-induced oxidative stress via targeting miR-27b-3p and thereby enhanced the antioxidant capacity by stimulating nuclear translocation and accumulation of Nrf2. These findings suggest that inhibition of miR-27b-3p to activate the Nrf2/ARE pathway by GEN is a potential alternative for hepatic oxidative damage alleviation.
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BIOMEDICINE & PHARMACOTHERAPY
·
2022
·
IF 7.419
Ya Zhang,Qifang Wu,Jian Liu,Zhongshan Zhang,Xiaojing Ma,Yaoyue Zhang,Jiawen Zhu,Ronald W. Thring,Mingjiang Wu,Yitian Gao,Haibin Tong
Insulin resistance is a characteristic feature of type 2 diabetes. Sulforaphane (SFN) is a natural antioxidant extracted from the cruciferous vegetables. Recent study reported that SFN exhibits excellent anti-diabetic effects, however, the underlying mechanism is still unclear. This study aimed to investigate the therapeutic effects of SFN on a high-fat diet (HFD)-induced insulin resistance and potential mechanism. SFN was found to effectively reduce body weight, fasting blood glucose and hyperlipidemia, and improve liver function in HFD-fed mice. Furthermore, SFN effectively increased glucose uptake and improved insulin signaling in palmitic acid (PA)-induced HepG2 cells. SFN also led to increased expression of antioxidant genes downstream of Nrf2 and decreased accumulation of lipid peroxides MDA and 4-HNE, both in vivo and in vitro. Further studies revealed that SFN significantly reduced glutathione peroxidase 4 (GPx4) inactivation-mediated oxidative stress by activating the AMPK and Nrf2 signaling pathways. In PA-induced HepG2 cells and flies , the alleviation of insulin resistance by SFN was diminished by GPx4 inhibitor. Taken together, SFN ameliorated HFD-induced insulin resistance by activating the AMPK-Nrf2-GPx4 pathway, providing new insights into SFN as a therapeutic compound for the alleviation of insulin resistance.
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ACTA HISTOCHEMICA
·
2020
·
IF 2.107
Xiaolong Sun,Xu Wang,Zhenyu Zhao,Jing Chen,Cheng Li,Gang Zhao
As one of the most frequent diabetic complications , diabetic foot ulcer (DFU) can cause limb ischemia or even amputation. Paeoniflorin (PF) has been reported to possess many kinds of biological functions, such as antioxidant and anti-inflammatory effects. However, the role of PF in DFU remains unknown. In this study, streptozotocin (STZ)-induced diabetic rat models and high glucose (HG)-treated Human immortalized keratinocytes (HaCaT) cells were established. Histological analysis, immunohistochemistry , Electrophoretic mobility shift assay , MTT assay , TUNEL assay , oxidative stress analysis, ELISA assay and western blot were used to investigate the role and underlying mechanisms of PF on healing in DFU. Our results showed that the STZ-induced diabetic rats had delayed wound healing compared with the normal rats, exhibited by intense oxidative DNA damage, low vascular endothelial growth factor (VEGF) and transforming growth factor β1 (TGF-β1) expression, as well as increased apoptosis . PF treatment activated the expression of nuclear factor-E2-related factor 2 (Nrf2) and improved wound healing in DFU rats. Our in vitro experiments confirmed that PF accelerated wound healing through the Nrf2 pathway under hyperglycemic conditions, with alleviated oxidative stress, increased cell proliferation and migration, decreased apoptosis, and increased the expression of VEGF and TGF-β1. Our study demonstrates the therapeutic benefits of PF in diabetic wound healing, which provides a reference for future clinical trials using PF in DFU treatment.
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MOLECULAR AND CELLULAR BIOCHEMISTRY
·
2020
·Vol. 473
·期 1
·217-228
·
IF 2.795
Wu Xinghan,Liu Chuanliang,Li Zihaoran,Gai Chengcheng,Ding Dejun,Chen Weijuan,Hao Fengyun,Li Wentong
Ferroptosis is a newly discovered form of regulated cell death and characterized by an iron-dependent accumulation of lethal lipid reactive oxygen species (ROS), ferroptosis may exhibit a novel spectrum of clinical activity for cancer therapy. However, the significance of ferroptosis in the context of carcinoma biology is still emerging. Glycogen synthase kinase-3β (GSK-3β) has been found to be a fundamental element in weaking antioxidant cell defense by adjusting the nuclear factor erythroid 2-related factor 2 (Nrf2). In our study, decreased expression of GSK-3β was observed in the cancer tissues of breast cancer patients, results of immunohistochemistry indicated that Nrf2 was highly expressed in low-GSK-3β-expressed breast cancer tissues. The contributions of aberrant expression of GSK-3β and Nrf2 to the erastin-induced ferroptosis in breast cancer were further assessed, silence of GSK-3β blocked erastin-induced ferroptosis with less production of ROS and malondialdehyde (MDA) via upregulation of GPX4 and downregulation of arachidonate 15-lipoxygenase (Alox15), overexpression of GSK-3β enhanced erastin-triggered ferroptosis with elevated ROS and MDA. Enhanced erastin-induced ferroptosis by overexpression of GSK-3β was blocked by activating Nrf2. We further confirmed that overexpression of GSK-3β strengthened erastin-induced tumor growth inhibition in breast cancer xenograft models in vivo. In summary, our findings conclude that modulation the balance between GSK-3β/Nrf2 is a promising therapeutic approach and probably will be important targets to enhance the effect of erastin-induced ferroptosis in breast cancer.
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FOOD AND CHEMICAL TOXICOLOGY
·
2019
·
IF 3.775
Maiquan Li,Weisu Huang,Fan Jie,Mengmeng Wang,Yongheng Zhong,Qi Chen,Baiyi Lu
Various phytochemicals have been reported to protect against oxidative stress. However, the mechanism underlying has not been systematically evaluated, which limited their application in disease treatment. Nuclear factor erythroid 2−related factor 2 (Nrf2), a central transcription factor in oxidative stress response related to numerous diseases, is activated after dissociating from the cytoskeleton−anchored Kelch−like ECH−associated protein 1 (Keap1). The Keap1–Nrf2 protein–protein interaction has become an important drug target. This study was designed to clarify whether antioxidantive phytochemicals inhibit the Keap1–Nrf2 protein–protein interaction and activate the Nrf2-ARE signaling pathway efficiently. Molecular docking and 3D−QSAR were applied to evaluate the interaction effects between 178 antioxidant phytochemicals and the Nrf2 binding site in Keap1. The Nrf2 activation effect was tested on a H 2 O 2 −induced oxidative−injured cell model. Results showed that the 178 phytochemicals could be divided into high−, medium−, and low−total−score groups depending on their binding affinity with Keap1, and the high−total−score group consisted of 24 compounds with abundant oxygen or glycosides. Meanwhile, these compounds could bind with key amino acids in the structure of the Keap1−Nrf2 interface. Compounds from high−total−score group show effective activation effects on Nrf2. In conclusion, phytochemicals showed high binding affinity with Keap1 are promising new Nrf2 activators.
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FOOD CHEMISTRY
·
2025
·
IF 9.8
Zaheer Abbas,Jing Zhang,Yucui Tong,Baseer Ahmad,Junyong Wang,Haosen Zhang,Zhenzhen Li,Xubiao Wei,Rijun Zhang,Dayong Si
The objective of this study was to isolate and characterize antioxidant peptides from mulberry leaves fermented with Bacillus subtilis H4 and Bacillus amyloliquefaciens LFB112. The results indicated that fraction F4 (<1 kDa) exhibited superior DPPH activity compared to the F1 (>10 kDa), F2 (3–10 kDa), and F3 (1–3 kDa) fractions, and cytoprotective effect against lipopolysaccharides (LPS)-induced oxidative stress in RAW264.7 cells. Three novel peptides, FRFDP, RFGG, and GPPLAFGGGP, were identified in the F4 fraction of the mulberry leaf ferment, and docking results showed that these peptides could form stable carbon (covalent) and hydrogen bonds to the active sites of Keap1, thus regulating the Keap1-Nrf2 pathway by blocking the Nrf2 binding sites on Keap1. These peptides significantly upregulated the mRNA expression of Nrf2 , HO-1 , and NQO1 , providing indirect evidence of their potential to enhance cellular antioxidant defense via the possible activation of Keap1-Nrf2 pathway. Furthermore, these peptides showed good DPPH and ABTS scavenging activities, indicating their potential as antioxidant peptides. This study offers valuable insights into the integration of these novel peptides in developing mulberry leaf ferment as a functional food and their potential use as a feed additive.
研究领域:
食品科学
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生物化学
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