PHYTOMEDICINE
·
2026
·
IF 11.3
Ludong Tan,Xiaodong Bai,Peiyuan Yu,Tinghan Jiang,Zhe Jin
Artemisia capillaris extract alleviates acetaminophen-induced liver injury by inhibiting ferroptosis. • Capillarisin is identified as the primary bioactive constituent responsible for the hepatoprotection. • Capillarisin directly binds to and inhibits Glycogen Synthase Kinase 3β (GSK3β). • Inhibition of GSK3β by Capillarisin activates the Nrf2-mediated anti-ferroptotic pathway. • This study reveals a novel molecular mechanism for a traditional hepatoprotective herb. Background Acetaminophen (APAP) overdose is a leading cause of acute liver failure worldwide, characterized by oxidative stress-driven hepatocyte necrosis. Recent evidence implicates ferroptosis, an iron-dependent cell death, as a critical pathogenic event. Artemisia capillaris Thunb. (ACE) is a traditional hepatoprotective herb; however, its bioactive constituents and molecular targets regulating ferroptosis remain elusive. Purpose This study aimed to identify the bioactive compounds of ACE and elucidate the molecular mechanism underlying its protective effect against APAP-induced hepatotoxicity, with a specific focus on the ferroptosis pathway. Methods We integrated multi-omics, network pharmacology, and rigorous biophysical assays to decipher the protective mechanism. The ethanol extract of A. capillaris was chemically characterized using UPLC-LTQ-Orbitrap MS. An APAP-induced acute liver injury model in C57BL/6 mice and primary mouse hepatocytes were employed. Transcriptomics (RNA-seq) was utilized to identify key signaling pathways. The direct physical interaction between the active compound and its target was validated using Microscale Thermophoresis (MST), Cellular Thermal Shift Assay (CETSA), Drug Affinity Responsive Target Stability (DARTS), and molecular dynamics (MD) simulations. Functional validation was performed using gene overexpression and specific inhibitors. Results ACE pretreatment significantly attenuated APAP-induced liver injury, inflammation, and oxidative stress in mice. Transcriptomic profiling identified ferroptosis as a primary target pathway. Through chemical screening, we identified Capillarisin as the key bioactive coumarin responsible for this effect. Capillarisin treatment effectively suppressed lipid peroxidation, iron overload, and the expression of ferroptotic markers (COX2, ACSL4) while restoring GPX4 levels both in vivo and in vitro . Mechanistically, we demonstrated that Capillarisin acts as a direct inhibitor of Glycogen Synthase Kinase 3β (GSK3β). Capillarisin binds stably to the ATP-binding pocket of GSK3β ( K d = 0.87 µM), thereby inhibiting its kinase activity. This inhibition blocks the phosphorylation-dependent degradation of Nrf2, promoting its nuclear translocation and the subsequent transcriptional activation of anti-ferroptotic genes ( Gpx4, Slc7a11 ). Overexpression of GSK3β or pharmacological inhibition of Nrf2 abolished the protective effects of Capillarisin. Conclusion Our study reveals a novel mechanism whereby Capillarisin alleviates APAP-induced hepatotoxicity by directly targeting GSK3β to activate the Nrf2-mediated anti-ferroptosis defense. These findings provide a rigorous scientific basis for the ethnopharmacological use of Artemisia capillaris and highlight Capillarisin as a promising lead candidate for targeting GSK3β in the treatment of drug-induced liver injury. Download: Download high-res image (228KB) Download: Download full-size image
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高影响因子
TOXICON
·
2026
·
IF 2.8
Jing Li,Xiaoxiao Wang,Liya Tu,Yufeng Chen
Ovarian cancer (OC) exhibits the highest mortality rate among gynecological cancers, and the development of chemotherapy resistance serves as the primary cause of patient recurrence and death. Natural products hold promise in reversing cisplatin (DDP) resistance. Trigonelline is a natural alkaloid possessing anti-tumor activity; however, it remains uncertain whether it can reverse DDP resistance in OC. In this study, DDP-resistant OC cell lines SKOV-3/DDP and A2780/DDP were successfully established. Cells were treated with non-toxic concentration of trigonelline in combination with DDP, and the molecular mechanism was investigated through the overexpression of Nrf2. Cell viability was detected to assess the sensitivity of the cells to DDP. Mitochondrial damage was evaluated by observing mitochondrial morphology, measuring mitochondrial membrane potential, ATP production, and ROS. Ferroptosis was assessed by detecting the levels of lipid peroxidation, MDA, SOD, Fe 2+ , and GSH/GSSG ratio in the cells. Additionally, the expression levels of ferroptosis-related proteins, namely Nrf2, HO-1, GPX4, and SLC7A11, were also detected. The results indicated that the utilization of low-concentration trigonelline exerted no toxic influence on OC drug-resistant cells, and instead potentiated the cytotoxicity of DDP against these cells. Furthermore, in comparison with the treatment using DDP alone, the combined treatment of trigonelline and DDP induced more severe mitochondrial damage and ferroptosis in drug-resistant cells. This led to the accumulation of ROS, notable increases in lipid peroxidation, MDA, and Fe 2+ levels within the cells, while decreasing SOD activity and the ratio of GSH/GSSG, and down-regulating the expression of Nrf2, HO-1, GPX4, and SLC7A11 proteins. Nevertheless, the overexpression of Nrf2 reversed the combined effect of trigonelline and DDP. These results indicate that trigonelline reverses DDP resistance in OC cells by promoting ferroptosis via the regulation of the Nrf2/GPX4 signaling pathway.
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高影响因子
Animals
·
2026
·Vol. 16
·期 12
·1828
·
IF 3.2
Junyu Wang,Min Li,Yaqi Zhou,Fuyin Fu,Feng Liu,Jinghe Tan,Mingjiu Luo,Shuai Gong
Simple SummaryPoor porcine oocyte and embryo quality limits pig breeding efficiency. This study tested metformin supplementation in culture media to improve oocyte maturation and embryo development. Low-dose metformin enhanced maturation and blastocyst formation by activating AMPK through a non-canonical pathway, reducing oxidative damage and improving mitochondrial function, while high doses impaired oocyte quality. Appropriate metformin use optimizes in vitro culture systems, supporting more efficient pig embryo production for agriculture and reproductive research.Metformin (MET) plays crucial regulatory roles in mammalian oocyte meiosis, yet the concentration-dependent biphasic impacts of MET on porcine oocyte in vitro maturation (IVM) and the related molecular mechanisms remain poorly clarified. This study aimed to explore the distinct effects and underlying pathways of low- and high-dose MET in porcine oocytes. Different concentrations of MET (0, 7.5, 15, 30, 150, and 300 μM) were supplemented during oocyte IVM, with phenotypic detection, untargeted metabolomic analysis, and Nrf2 inhibitor (ML385) intervention performed for mechanism exploration. Results showed that 15 μM low-dose MET facilitated oocyte maturation, mitochondrial function and redox balance, while 300 μM high-dose MET caused obvious developmental damage. Mechanistically, low-dose MET triggered noncanonical AMPK activation independent of the AMP/ATP ratio and enhanced AMPK–Nrf2 antioxidant signaling, whereas high-dose MET induced energy stress and oxidative injury via inhibiting mitochondrial complex I. Blockade of Nrf2 further abolished the protective effects of low-dose MET. Collectively, this finding illustrates the biphasic actions of MET on porcine oocytes and provides a theoretical reference for optimizing porcine in vitro embryo production.
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高影响因子
Reproductive Biology
·
2026
·Vol. 26
·期 3
·101239
·
IF 2.5
Jing Wu,Yu Zeng,Xianyan Xiong,Hongmei Zhu
Preeclampsia (PE, a pregnancy-specific hypertensive disorder) is characterized by placental hypoxia, oxidative stress, metabolic dysfunction, and trophoblast impairment, yet effective disease-modifying therapies remain limited. Although low-dose aspirin (Acetylsalicylic acid, ASA) is recommended for the prevention of PE and has shown protective effects in pregnancy, the underlying placental mechanisms remain incompletely understood. Nuclear factor erythroid 2–related factor 2 (NRF2), a central regulator of cellular antioxidant defense, plays a critical role in counteracting oxidative stress, but its role in placental pathology and its contribution to ASA-mediated protection in PE have not been fully elucidated. In this study, placental tissues were collected from normotensive pregnancies and from patients with mild and severe PE, and relevant maternal clinical characteristics were recorded to contextualize findings. In parallel, trophoblast cells were exposed to physiological hypoxia or hydrogen peroxide (H₂O₂)–induced oxidative stress to mimic PE-relevant placental stress conditions, followed by ASA treatment. Trophoblast function, oxidative stress, and apoptosis were evaluated, and the involvement of NRF2 was examined using shRNA-mediated knockdown. Placental tissues from PE pregnancies, particularly those from severe cases, exhibited increased oxidative stress accompanied by dysregulated NRF2-dependent antioxidant signaling. In vitro, both hypoxia and oxidative stress significantly impaired trophoblast proliferation and invasion while increasing reactive oxygen species (ROS) accumulation and apoptosis. ASA treatment markedly reduced oxidative stress and improved trophoblast function under both stress conditions. Notably, genetic silencing of NRF2 largely abolished the antioxidative and cytoprotective effects of ASA. These findings indicate that ASA alleviates placental oxidative injury and trophoblast dysfunction, at least in part, through an NRF2-dependent mechanism, providing mechanistic insight into the placental protective effects of ASA in PE and highlighting the potential clinical relevance of ASA for high-risk pregnancies.
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高影响因子
PHYTOMEDICINE
·
2026
·
IF 11.3
Bing Yu,Lina Zhang,Jing Lin,Qian Wang,Menghui Chi,Ziyi Wang,Wenyao Liu,Shan Wang,Zhipeng Wei,Cui Li,Guiqiu Zhao
Background Fungal keratitis is a vision-threatening corneal disease, in which uncontrolled inflammation and oxidative damage often result in poor clinical outcomes. Current antifungal drugs exert fungicidal activity but often fail to control inflammatory injury, limiting their therapeutic efficacy. Therapies capable of enhancing fungal clearance while modulating host inflammation are urgently needed. Farrerol (FA), a natural flavanone, has anti-inflammatory, antioxidant, and antimicrobial properties, yet its role in fungal keratitis remains unclear. Purpose To investigate the therapeutic effects and mechanisms of FA in Aspergillus fumigatus -induced keratitis. Methods RT-qPCR, Western Blot, Co-IP, ELISA, and immunofluorescence staining were performed to assess the effects of FA on inflammatory responses and oxidative stress in fungus-stimulated macrophages. MIC assay, Calcofluor White staining, and plate counting method were used to examine the antifungal activity. A murine fungal keratitis model was established to determine the therapeutic efficacy in vivo . Results FA significantly alleviated corneal inflammation and fungal burden in vivo . Mechanistically, FA enhanced autophagic flux and promoted autophagy-dependent degradation of Keap1, resulting in Nrf2 nuclear translocation. The activation of autophagy and Nrf2 feedback loop suppressed the production of pro-inflammatory cytokines and ROS while enhancing macrophage-mediated intracellular killing of conidia. Inhibition of autophagy abolished these protective effects. Conclusions FA protects against fungal keratitis by enhancing fungal clearance and limiting excessive inflammation through activation of autophagy and the Nrf2 pathway. These findings identify FA as a promising therapeutic candidate and highlight autophagy–Nrf2 signaling as a potential target in fungal infectious diseases.
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高影响因子
PHYTOMEDICINE
·
2026
·
IF 11.3
Xiaojue Xiang,Xu Lin,Qifang Wu,Xiaoming Zhang,Xueliang Fu,Linya Wu,Haibin Tong,Zhenyu Dai
Dendrobium officinale extract DOE ameliorates metabolic disorders and diabetic cardiomyopathy. • DOE reduced myocardial injury, fibrosis, and oxidative stress via activating NRF2 pathway. • Dendrobine was the principal cardioprotective alkaloid in DOE against diabetic cardiomyopathy . • Dendrobine directly targets KEAP1 Kelch domain to disrupt the KEAP1-NRF2 interaction . Background Dendrobium officinale Kimura et Migo is a prestigious traditional Chinese medicine historically used for treating "Xiao-Ke" (diabetes and its complications). However, the specific material basis and direct molecular targets responsible for its efficacy against diabetic cardiomyopathy (DCM) remain largely obscure. This study aimed to systematically investigate whether dendrobine, the characteristic active alkaloid of DO, serves as the principal cardioprotective component by directly targeting the KEAP1-NRF2 signaling axis. Methods The therapeutic effects of D. officinale extract (DOE) and dendrobine were evaluated in vivo using db/db mice and in vitro using high-glucose (HG)-challenged H9c2 cardiomyocytes. Cardiac pathological remodeling, lipid peroxidation, and systemic metabolic profiles were comprehensively assessed. The direct interaction between dendrobine and KEAP1 was definitively characterized using Co-Immunoprecipitation (Co-IP), Cellular Thermal Shift Assay (CETSA), Drug Affinity Responsive Target Stability (DARTS), MicroScale Thermophoresis (MST), and 100-ns Molecular Dynamics (MD) simulations. Reverse pharmacological validation was performed using NRF2-specific siRNA and the inhibitor ML385. Results In vivo , DOE significantly ameliorated systemic insulin resistance, hyperlipidemia, and myocardial pathological remodeling in db/db mice while robustly suppressing myocardial oxidative stress (MDA, 4-HNE) by upregulating NRF2-driven antioxidant enzymes (HO-1, NQO1, GPX4). In vitro , dendrobine dose-dependently replicated these cardioprotective and antioxidative efficacies. Mechanistically, dendrobine promoted NRF2 nuclear translocation and initiated the downstream antioxidant cascade. Crucially, MST and CETSA revealed that dendrobine binds directly to KEAP1 with high affinity ( K d = 1.18 μM), functioning as a competitive protein-protein interaction (PPI) inhibitor to disrupt the KEAP1-NRF2 complex. MD simulations and mutagenesis validation pinpointed the Kelch domain of KEAP1 (specifically residue Arg415) as the binding pocket. Finally, silencing or inhibiting NRF2 abolished the anti-hypertrophic and cytoprotective effects of dendrobine, and the in vivo administration of dendrobine successfully recapitulated the metabolic regulation and KEAP1/NRF2-mediated cardioprotection of DOE in db/db mice. Conclusion Dendrobine, the principal alkaloid of D. officinale , effectively ameliorates diabetic cardiomyopathy by functioning as a novel, direct competitive inhibitor of the KEAP1-NRF2 interaction. This targeted disruption liberates NRF2 to restore myocardial redox homeostasis, highlighting dendrobine as a promising lead compound for DCM therapy. Download: Download high-res image (395KB) Download: Download full-size image
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Emerging Contaminants
·
2026
·Vol. 12
·期 4
·100770
·
IF 8.2
Si Dong,Yunyun Du,Yongliang Zheng,Ting Ding,Zhonghao Xiao,Suwei He,Shanshan Zhu,Yulian Li,Wenfeng He,Xiaoping Wang,Lingci Zeng,Fasheng Liu,Junquan Zeng
Hematotoxicity and immunotoxicity are common adverse effects observed in fish exposed to environmental pollutants; however, the molecular mechanisms underlying these toxicities remain poorly understood. To investigate these mechanisms, zebrafish were exposed to dicofol (DCF) under environmentally relevant conditions. DCF exposure led to increased reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT), and reduced nitric oxide (NO) content. Further analysis revealed a significant increase in TUNEL-positive cells in hematopoietic regions, accompanied by elevated expression of Bax/Bcl-2 , caspase-3 , and p53 . Antibody staining and Western blot (WB) analysis demonstrated that DCF impaired the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant system. Astaxanthin (AST) treatment alleviated DCF-induced damage to hematopoietic stem cells. These results show that DCF disrupts antioxidant homeostasis, aggravates oxidative stress, and ultimately triggers apoptosis in hematopoietic stem cells, offering new insights into strategies to prevent and control pollutant-induced toxicity.
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高影响因子
AQUACULTURE NUTRITION
·
2025
·Vol. 2025
·期 1
·6665220
·
IF 3.9
Shiping Yang,Leyuan Feng,Junliang Luo,Jichang Jian,Shuanghu Cai,Huiling Liu
Nuclear factor erythroid 2-related factor 2 (Nrf2) is an essential component in regulating oxidative stress. Sulforaphane (SFN) is a natural antioxidant and gene Nrf2 agonist that can increase the antioxidant capacity of the organism and reduce oxidative stress. However, research on the repair of oxidative stress damage by SFN in aquatic animals remains extremely scarce. In order to further explore the function and role of SFN in the repair of oxidative stress injury in aquatic animals, this study took Litopenaeus vannamei as the research object. We established an oxidative stress model of L. vannamei through 6% oxidized fish oil (OFO) feeding. Methods, such as RNA interference (RNAi), qPCR, histopathological analysis, and TUNEL assay, were used to detect the changes in the oxidative stress status of L. vannamei . The results showed that the expression of Nrf2 in the hepatopancreas of L. vannamei in the double-stranded RNA (dsRNA)- Nrf2 + SFN group was significantly higher than that in the dsRNA- Nrf2 group and control group at 24 h ( p < 0.05). The transcription levels of antioxidant and autophagy genes in the SFN group were significantly higher than those in the control group ( p < 0.05), and the expression of related genes in the dsRNA- Nrf2 + SFN group was also higher than that in the dsRNA- Nrf2 group. Histopathology showed that Nrf2 knockdown would aggravate hepatopancreatic apoptosis and vacuolation, while SFN treatment after Nrf2 knockdown could alleviate hepatopancreatic injury and apoptosis caused by OFO. The results indicated that SFN could repair the oxidative stress injury of L. vannamei induced by OFO by activating Nrf2 . This study investigated the role of SFN in alleviating and repairing the oxidative stress damage in L. vannamei caused by OFO, aiming to provide a theoretical basis for the research on the antioxidant effect of SFN and the regulation of the antioxidant capacity of shrimp.
研究领域:
海洋生物学
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水产养殖
·
分子生物学
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毒理学
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药理学
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2026
·
IF 6.7
Caiyan Zhang,Fengxian Sui,Meiyan Liu,Yalin Xie,Jiadi Su,Jing Gao,Ye Lin,Yang Yang,Xiaoming Hou
Oleic acid (OA)-enriched diet significantly enhances CD36 expression and promotes milk fat production in the mammary gland. However, the mechanisms by which OA upregulates this process are unknown. Here, GC-MS analysis and molecular docking were used to assess OA-CD36 binding, while gene expression and ChIP assays clarified the OA-mediated regulation of CD36 and milk fat synthesis. The results showed that CD36 is highly expressed in the lactating mammary tissues of dairy cows and positively regulates milk fat production. OA enters dairy cow mammary epithelial cells via direct binding to CD36. OA stimulation elevates the CD36 expression and translocation. ChIP assays confirmed CD36 as a target gene of NRF2. OA also enhances NRF2 expression and nuclear translocation, which in turn upregulates CD36 expression and function. This study elucidates the NRF2–CD36 axis as a regulator of OA-driven milk fat synthesis in mammary tissue, offering practical value for dairy industry nutritional strategies.
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高影响因子
RENAL FAILURE
·
2026
·
IF 3.8
Jia Wang,Jin-Wei E.,Jiong Zhang
Roxadustat (ROX) has a protective action against contrast-induced acute kidney injury (CI-AKI). Excessive production of reactive oxygen species (ROS) plays a significant role in exacerbating the deterioration of renal function. Notably, activation of Nrf2/HO-1 signaling can reduce ROS production. We constructed a mouse model of CI-AKI by iohexol injection. The effect of ROX on CI-AKI was assessed by measuring serum blood urea nitrogen (BUN) and creatinine (Cr), evaluating renal histopathology, and analyzing the expression level of Nrf2 and HO-1. Additionally, levels of ROS, malondialdehyde (MDA), proinflammatory cytokines (IL-6, TNF-α, and IL-1β), as well as the activities of antioxidant kinases superoxide dismutase (SOD) and glutathione (GSH), were examined. The results showed that ROX significantly suppresses the iohexol-induced decline in the activity of antioxidant enzymes, increases the levels of ROS, MDA, Cr, IL-6, IL-1β, BUN and TNF-α, and attenuates renal pathological injury. Furthermore, ROX enhanced the iohexol–induced increase in Nrf2 and HO-1 expression. However, these effects of ROX on CI-AKI were abolished by ML-385, a Nrf2 inhibitor. Our findings indicate ROX attenuates CI-AKI by down-regulating inflammation and restoring the balance between oxidative stress and anti-oxidant defenses. This may involve the activation of the Nrf2/HO-1 signaling pathway to clear excessive ROS.
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高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·Vol. 24
·期 1
·391
·
IF 15
Chen Ying,Peng De-Wei,Jiang Sheng-Rui,Shao Qian-Chun,Zhang Yi-Cong,Chi Zai-Long
Objective Retinal neovascularization is a leading cause of irreversible blindness worldwide. Chinese herbal medicines have unique therapeutic properties, such as antioxidant, anti-inflammatory, and neuroprotective effects. This study aims to investigate the therapeutic effects and underlying mechanisms of the Chinese medicinal herb Curcuma longa -derived extracellular vesicle-like particles (CL-EVLPs) in a mouse model of retinal neovascularization. Methods CL-EVLPs were extracted from fresh Curcuma longa rhizomes through differential centrifugation and sucrose density gradient centrifugation and characterized by transmission electron microscopy (TEM), and nanoparticle tracking analysis (NTA), and western blot analysis of EVLP-associated protein markers. CL-EVLPs were administered to oxygen-induced retinopathy (OIR) model mice via intravitreal injection. The therapeutic effects were evaluated using retinal flat mounts, fundus fluorescein angiography (FFA), and reactive oxygen species (ROS) staining. The underlying molecular mechanisms were explored through metabolomics, transcriptomics, and network pharmacology analyses, and the expression levels of relevant factors were quantified using real-time polymerase chain reaction (PCR) or western blotting. In vitro experiments were conducted using human retinal microvascular endothelial cells (hRMECs) and BV2 microglia. Results CL-EVLPs exhibited typical EV-like characteristics, including a saucer‑ or cup‑shaped morphology, a mean diameter of 140.7 nm, and enrichment of the EV‑related protein ARF1. CL-EVLPs effectively inhibited neovascularization in the OIR model, as evidenced by reduced pathological neovascular tufts and avascular zones and decreased vascular permeability and tortuosity. Furthermore, CL-EVLPs significantly decreased ROS production in the retinas of OIR mice. Mechanistically, CL-EVLPs inhibited HIF-1α/VEGF/ERK signaling and activated the NRF2/HO-1 antioxidant pathway. In vitro experiments confirmed that CL-EVLPs inhibited endothelial cell viability and alleviated oxidative stress in microglia. Integrated network pharmacology and metabolomics analyses proved that the cargo molecules of CL-EVLPs, such as curcumin and its derivatives, auraptene, and triptophenolide, exhibit regulatory antioxidant and anti-inflammatory effects and modulate multiple signaling pathways associated with retinal neovascular diseases. Conclusion CL-EVLPs effectively suppress retinal neovascularization by inhibiting the HIF-1α/VEGFA/ERK axis and activating the NRF2/HO-1 pathway. This study suggests that CL-EVLPs, as a multitarget therapeutic strategy, hold promising clinical translational potential for the treatment of retinal neovascular diseases. Graphical abstract The alternative text for this image may have been generated using AI.
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高影响因子
Aging-US
·
2018
·
IF 5.179
Xingting Liu,Xin Lin,Siyu Zhang,Changquan Guo,Jian Li,Yuling Mi,Caiqiao Zhang
After 480 days of age, high-producing hens are likely to be subject to ovarian aging, mainly due to oxidative stress. In this study, the amelioration of ovarian aging in chickens, using a plant antioxidant, lycopene, was investigated. The activity of the Nrf2/HO-1 pathway in chicken ovaries at different ages (90, 150, 280 and 580 days old) were compared to elucidate any age-related changes. Subsequently, the putative attenuating effect of lycopene (100 ng/mL) on ovarian aging was evaluated through the establishment of a D-gal-induced aging ovarian culture model. The cultured ovarian tissues of young (280 days) and old (580 days) hens were treated with lycopene for 72 h to verify protective effects of lycopene on naturally aged ovaries. Results showed that the Nrf2/HO-1 pathway was down-regulated during the ovarian aging process. Lycopene rescued the decreased antioxidant capacity by increasing the activities of antioxidases and activating the Nrf2/HO-1 pathway in both D-gal-induced and naturally aged ovaries. Moreover, lycopene promoted cell proliferation and inhibited apoptosis in both D-gal-induced and naturally aged ovaries. Lycopene also alleviated D-gal-induced mitochondrial damage in the living granulosa cells. In conclusion, lycopene can effectively ameliorate the oxidative stress in aging hen ovaries via the activation of the Nrf2/HO-1 pathway.
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高影响因子
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