Current Research in Food Science
·
2022
·
IF 6.269
Yong Chen,Jiajun Wang,Ziheng Jing,Jose M. Ordovas,Jing Wang,Lirong Shen
Demands for dietary supplements with anti-fatigue effects are growing fast due to increasing societal demands. Moreover, in highly physically active individuals, there are also significant needs for supplements to improve exercise performance. The present study evaluated the potential anti-fatigue and anti-oxidant effects of curcumin in mice using exhaustive swimming test. Male C57BL/6J mice were randomized into six groups: blank control (Rest), swimming control (Con), Vitamin C (Vc), low-dose curcumin (C 50 ), middle-dose curcumin (C 100 ), and high-dose curcumin (C 200 ). After a 4-week intervention, the mice in all groups except the Rest group were subject to an exhaustive swimming test. Then, mice were sacrificed to examine serum biochemical markers and fatigue-related enzymes. Moreover, the gene and protein expressions of signal transduction factors involved in the Nrf2/Keap1 signaling pathway were measured. The results indicated that curcumin significantly enhanced the exercise tolerance of mice in the exhaustive swimming test. Particularly, the swimming time of mice in the C 100 group was increased by 273.5% when compared to that of mice in the Con group. The levels of blood urea nitrogen, blood ammonia, lactic acid, creatine kinase and lactate dehydrogenase in the C 100 group were decreased by 13.3%, 21.0%, 18.6%, 16.7% and 21.9%, respectively, when compared to those of mice in the Con group. Curcumin alleviated exercise-induced oxidative stress and significantly enhanced the activities of superoxide dismutase, catalase and glutathione peroxidase by activating the Nrf2 signaling. These findings indicated that curcumin supplementation exerted remarkable anti-oxidant and anti-fatigue effects in mice, providing additional evidence supporting the use of curcumin as functional food, especially by those engaged in sports-related activities.
研究领域:
营养学
·
运动生理学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
NEUROCHEMISTRY INTERNATIONAL
·
2025
·
IF 4
Yinpei Huang,Hailun Xie,Lian Liu,Heng Zhao,Bing Li,Feng Zhang
Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (IH), which induces oxidative stress and neuronal apoptosis, ultimately leading to progressive cognitive impairment. This study investigated the neuroprotective potential of a reactive oxygen species (ROS)-responsive nanotherapeutic, namely TPCD nanoparticles (TPCD NP), synthesized through the conjugation of Tempol and phenylboronic acid pinacol ester to β-cyclodextrin, in both in vivo and in vitro models. In rats, intravenous administration of TPCD NP improved memory performance as assessed by the Morris water maze test, and preserved hippocampal neuronal morphology. TPCD NP significantly reduced intracellular ROS content and malondialdehyde (MDA) levels while restoring antioxidant capacity, including superoxide dismutase (SOD) and glutathione (GSH). Apoptosis was attenuated, as evidenced by the downregulation of Bax and cleaved caspase-3, and the upregulation of Bcl-2 expression. Mechanistically, TPCD NP enhanced the nuclear translocation of nuclear factor erythroid 2–related factor 2 (NRF2), suppressed Kelch-like ECH-associated protein 1 (KEAP1), and increased heme oxygenase-1 (HO-1) expression. The protective effects were abolished by ML385, a selective NRF2 inhibitor, confirming the essential role of NRF2 activation in mediating the antioxidant and anti-apoptotic effects of TPCD NP. In conclusion, TPCD NP attenuates oxidative stress and apoptosis induced by IH in the hippocampus by activating the NRF2/KEAP1/HO-1 pathway. These findings highlight TPCD NP as a promising therapeutic strategy for OSA-associated neurodegeneration.
研究领域:
医学
·
神经科学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULAR AND CELLULAR BIOCHEMISTRY
·
2022
·Vol. 478
·期 2
·241-247
·
IF 3.842
Zhou Quan,Cai Xu,Huang Ying,Zhou Youliang
Curcumin (CUR) is an extract of Curcuma longa Linn., which has various pharmacological activities. The instability, low water solubility and bioavailability of CUR greatly limit its clinical application. This work prepared Pluronic F127-liposome-encapsulated curcumin (CUR-LIP-F127) and explored its functional role in wound healing. Liposome-encapsulated curcumin (CUR-LIP) and CUR-LIP-F127 were prepared. Human keratinocyte cell line (HaCaT) was treated with CUR, Pluronic F127-liposome (LIP-F127) and CUR-LIP-F127, or combined with ML385 (Nrf2 inhibitor). The expression of mRNAs and proteins was detected by quantitative real-time PCR and western blotting. MTT and wound healing assays were performed to detect cell viability and migration. CUR, LIP-F127 and CUR-LIP-F127 all had no influence on cell viability of HaCaT cells. CUR-LIP-F127 treatment significantly accelerated cell migration and enhanced the expression of nuclear factor erythroid-related factor 2 (Nrf2) and kelch-like erythroid cell-derived protein 1 (Keap1) in HaCaT cells with respect to CUR or LIP-F127 treatment. ML385 treatment impaired CUR-LIP-F127-mediated promotion of migration and up-regulation of Nrf2 and Keap1 in HaCaT cells. This work demonstrated that CUR-LIP-F127 activated Nrf2/Keap1 signaling pathway to promote migration of HaCaT cells, suggesting that CUR-LIP-F127 may contribute to wound healing.
研究领域:
药理学
·
细胞生物学
·
材料科学
·
生物医学工程
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food & Function
·
2016
·Vol. 7
·期 11
·4683-4692
·
IF 2.686
Fan Yuan-jing,Wei Wei,Luo Jian-ping,Jin Yu-xia,Dai Zi-ling
This study aimed to explore the effects of genistein on regulating the activation of UGTs via the Nrf2/Keap1 pathway and to elucidate the underlying mechanisms of detoxification and hepatic protection. Experiments monitoring genistein-induced protection against acetaminophen-induced cell damage were performed in L-02, HepG2 and Hep3b cells. The results of the MTT, AST, ALT, LDH, GSH and GSSG assays showed that genistein evidently protected the cells from acetaminophen-induced injury in a dose-dependent manner. The control cells were treated with 10 mM acetaminophen without genistein to compare with the effects of the combination of acetaminophen and genistein on the expression of UGT1A1, 1A6 and 1A9, Nrf2 and Keap1 mRNAs, as well as the expression of Nrf2 and Keap1 proteins, which were tested by western blotting. The results showed that the expression of the Nrf2 mRNA and protein increased; in contrast, the expression levels of the Keap1 mRNA and protein were obviously reduced by genistein in a dose-dependent manner. Meanwhile, the expression of the UGT mRNA was increased, and UGT1A9 exhibited the highest expression among the three UGTs. Accordingly, the residual acetaminophen content was obviously reduced and acetaminophen glucuronidation increased after 24 hours of treatment with genistein in a dose-dependent manner.
研究领域:
药理学
·
毒理学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
TISSUE & CELL
·
2023
·
IF 2.6
Lei Huang,Mengxuan Bian,Shunyi Lu,Jiayi Wang,Jieqin Yu,Libo Jiang,Jian Zhang
Ferroptosis is a novel form of cell death, which is a unique modality of cell death and closely associated with iron concentrations, generation of reactive oxygen species (ROS), and accumulation of the lipid reactive oxygen species. In the present study, the anti-ferroptosis effects of Engeletin was studied in erastin-induced bone marrow mesenchymal stem cells (BMSCs). After treatment with Engeletin, cell viability was determined by CCK-8 assay. The production of ROS, malonaldehyde (MDA), Superoxide dismutase (SOD) activities and glutathione peroxidase (GSH) were detected by using commercially-available kits. Ferroptosis-related proteins (GPX4, SLC7A11, TFR1, FPN1, Nrf2, Keap1) were evaluated by Western blotting. Osteogenic capacity was evaluated by ALP staining and ARS staining. The expression of osteogenic-related proteins (OPN, Runx2, OCN) were evaluated by Western blotting and changes in mRNA (ALP, BMP-2, COL-1, Osterix) were evaluated by RT-PCR. Consistent improvements in angiogenesis are observed with Engeletin in the presence of erastin. Engeletin significantly alleviated erastin-induced oxidative damage and protected against ferroptosis in BMSCs. Ferroptosis was inhibited by Engeletin, leading to decreasing reducing accumulation of ROS and lipid peroxidation products. Moreover, Engeletin promoted osteogenic differentiation in BMSCs and angiogenesis in human umbilical vein endothelial cells (HUVECs). Taken together, these findings indicate that Engeletin can protect BMSCs from erastin-induced ferroptosis through the Nrf2/Keap1 antioxidant pathway and identify Engeletin as a novel ferroptosis inhibitor, suggesting that Engeletin may promote resistance to ferroptosis and enable osteogenic function of BMSCs.
研究领域:
细胞生物学
·
药理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Foods
·
2025
·Vol. 14
·期 10
·1707
·
IF 5.1
Li Li,Ying Hu,Yu-Mei Wang,Xiao-Xue Wu,Si-Tong Lin,Hang Li,Ji Zhang,Guo-Rong Fan,Zong-De Wang,Bin Wang,Shang-Xing Chen
In this study, we systematically investigated the mechanisms of the antioxidation and anti-lipid accumulation effects of antioxidant peptides fromLitsea cubebaon a free fatty acid (FFA)-induced NAFLD model of HepG2 cells. The NAFLD cell model was constructed by inducing the HepG2 hepatocellular carcinoma cell line with 0.5 mmol/L FFAs, and AQRDAGLL, QEGPFVR, and DVPPPRGPL were given to the culture to study their lipid-lowering and antioxidant activities on NAFLD cells. The lipid-lowering activities of the three antioxidant peptides were evaluated by Oil Red O staining and TG and TC content assays, and the results showed that all three peptides had strong ameliorating effects on FFA-induced lipid accumulation in NAFLD cells. The intracellular antioxidant protease (CAT, GSH, and SOD) activity levels and lipid peroxidation (MDA) content were measured and intracellular ROS levels were detected. The results showed that after intervention with the antioxidant peptides, the intracellular ROS levels in the NAFLD model cells were significantly reduced, the SOD and CAT activities were increased, the GSH content was elevated, and the MDA content was reduced, which indicated that AQRDAGLL, QEGPFVR, and DVPPPRGPL were able to inhibit the oxidative stress of the cells effectively and to achieve the effect of intervening in NAFLD. JC-1 fluorescence staining experiments showed that the mitochondrial membrane potential function of NAFLD cells was restored under the effect of the antioxidant peptides. Molecular dynamics simulations revealed that the main driving force between QEGPFVR and Keap1 protein was van der Waals forces, ΔG = −62.11 kcal/mol, which indicated that QEGPFVR was capable of spontaneously binding to Keap1 protein.
研究领域:
生物化学
·
分子生物学
·
医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
·
2023
·
IF 4.7
Guanglu Wang,Jiajia Guo,Yeyun Ma,Yue Xin,Xiaomeng Ji,Ying Sun,Jian Zhang,Jingquan Dong
The increasing concern over environmental pollution caused by the pesticide avermectin used in aquaculture has attracted significant attention. The use of avermectin, a neurotoxic pesticide, in aquatic environments leads to toxic effects on non-target organisms, particularly causing harm to fish. The phenolic compound ferulic acid possesses excellent anti-inflammatory and antioxidant capabilities. This study was conducted by establishing a chronic exposure experiment to avermectin, proposes the use of ferulic acid as a dietary additive to protect the carp brain from damage caused by exposure to avermectin. Furthermore, it investigates the anti-inflammatory and antioxidant effects of ferulic acid in the carp brain under chronic exposure to avermectin. The experimental results demonstrate that ferulic acid can alleviate brain tissue inflammation and oxidative stress by modulating the Nrf2/Keap1 and NF-κB signaling pathways . It protects the carp brain from chronic avermectin-induced damage, preserves the integrity of the carp blood-brain barrier, enhances the levels of feeding factors, and thereby alleviates carp growth inhibition. These findings provide new therapeutic strategies and a theoretical foundation for the sustainable development of carp aquaculture.
研究领域:
水产养殖
·
毒理学
·
药理学
·
神经科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF FOOD SCIENCE AND TECHNOLOGY
·
2024
·Vol. 59
·期 9
·6231-6242
·
IF 2.6
Mengmeng Zhang,Tianchui Wang,Sixian Ou,Yucong Zou,Xuan Xin
Summary Betaine is a natural antioxidant lacking the ability to scavenge free radicals. Although it has been shown to exert antioxidant function by enhancing the expression of antioxidant enzymes, its mechanism has not yet been elucidated. This study explored the role and mechanism of the transcription factor NF-E2-associated factor 2 (Nrf2)-Kelch-like epichlorohydrin-associated Protein 1 (Keap1) antioxidant reaction element (ARE) pathway in betaine-mediated enhancement of antioxidant enzyme expression. Results derived from real-time quantitative PCR, Western blot, quantitative methylation-specific PCR, and inhibitors assay experiments showed that betaine activated the Nrf2-Keap1-ARE pathway, leading to an increase in the mRNA level of superoxide dismutase, glutathione peroxidase, and heme oxygenase-1. The mechanism may involve betaine's promotion of DNA methyltransferase expression, resulting in increased methylation of Keap1 DNA promoter, which ultimately reduces the level of Keap1 mRNA. Therefore, betaine can directly activate the Nrf2-Keap1-ARE pathway by increasing the methylation level of Keap1 DNA promoter, thereby improving the expression of antioxidant enzymes. This study will contribute to unveiling a new antioxidant mechanism for betaine.
研究领域:
分子生物学
·
药理学
·
生物化学
✓ 已验证
产品关联
DOI
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Ji Liu,Ying Han,Zhiyun Wu,Manli Chen,Wenwen Wu,Zijun Zhao,Jinjin Yuan,Zhijian Zheng,Qiang Lin,Nan Liu,Hongbin Chen
Background Perilladehyde, an extract of perillae in the Labiatae family, can produce significant anti-inflammatory and antioxidant effects. Although literature evidences the favorable effect of perillaldehyde on ischemic stroke, the exact mechanism remains blurred. Purpose This study attempted to explore the impact of perillaldehyde on cerebral ischemia-reperfusion injury and the related action mechanism. Methods The rat tMCAO and neuronal OGD/R models were established to simulate cerebral ischemia-reperfusion injury. Lentiviruses were used to interfere with the expression of Nrf2 and Trx2 in neurons. The effects and action mechanisms of perillaldehyde were explored by various experimental methods, including chromatin immunoprecipitation assay, Western Blot, flow cytometry, dual-luciferase reporter gene assay, transmission electron microscopy, MRI, RNA-seq, and immunofluorescence staining. Results Perillaldehyde pretreatment effectively mitigated the tMCAO-induced brain injury in rats by reducing cerebral infarction, improving neuromotor function, and attenuating cell apoptosis in the ischemic penumbra. In vitro, perillaldehyde pretreatment alleviated cell death and excessive oxidative stress, preserved the mitochondrial membrane integrity, enhanced mitochondrial energy metabolism, and facilitated the restoration of mitochondrial ultrastructure after OGD/R. The mechanism probe revealed that perillaldehyde activated the Nrf2/Keap1/Trx2 signaling axis, thus promoting the transcription of Trx2 and improving mitochondrial structure and function. The aforementioned impacts of perillaldehyde were somewhat counteracted by disrupting the expression of Nrf2 and Trx2, suggesting that the neuroprotection of perillaldehyde partially involves the activation of the Nrf2/Keap1/Trx2 axis. Conclusions This study firstly demonstrates the existence of the Nrf2/Keap1/Trx2 signaling axis in cerebral ischemia-reperfusion injury and evidences that perillaldehyde pretreatment can promote the restoration of neuronal mitochondrial structure and function by activating the Nrf2/Keap1/Trx2 axis after cerebral ischemia-reperfusion injury. These findings signify that perillaldehyde holds great promises for clinical management of ischemic stroke.
研究领域:
神经科学
·
药理学
·
分子生物学
·
医学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOLOGICAL RHYTHM RESEARCH
·
2023
·
IF 1.1
Xing-Chen Wang,Zhe Wang,Chuan-Li Wang,Hui-Liang Xue,Ming Wu,Lei Chen,Chao Fan,Jin-Hui Xu,Lai-Xiang Xu
Changes in photoperiod affect both oxidative stress (OS) levels and antioxidant enzyme activities in animals. The liver accounts for a vital body metabolic organ. Different light durations may produce different outcomes in terms of OS and liver antioxidant pathways, but the underlying mechanism is not yet understood. This study investigated the effects of diverse photoperiods (SD, short day; MD, moderate day; LD, long day) on OS degree (H2O2 and MDA), antioxidant enzyme activities (superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx]), liver total antioxidant capacity, and the Nrf2-Keap1 signaling pathway in striped dwarf hamsters (Cricetulus barabensis) livers. Our results showed that (1) SD treatment for 8 weeks increased the levels of phosphorylated Nrf2, upregulated the Nrf2-Keap1 signaling pathway, and increased the protein expression of SOD and GPx, while decreasing the MDA concentration, all of which reduced the OS degree. (2) Additionally, LD treatment for 8 weeks reduced the extent of Nrf2 phosphorylation, resulting in downregulation of the Nrf2-Keap1 pathway, thus reducing protein expression of SOD2 and CAT, increasing the concentrations of H2O2 and MDA, and increasing OS degree. Collectively, OS levels in C. barabensis liver decreased during SD but increased during LD.
研究领域:
生理学
·
分子生物学
·
生物化学
✓ 已验证
产品关联
DOI
高影响因子
Journal of Inflammation Research
·
2025
·
IF 4.1
Bingyan Gu,Yuying Chen,Huifang Xu,Kunyu Zhan,Keying Zhu,Huan Luo,Yanqun Huang,Hanbing Zeng,Wenbiao Zheng,Kun Tian,Hongfeng Ruan
Purpose Chlorpyrifos (CPF), a widely used organophosphate pesticide in agriculture, particularly in China, has raised significant environmental and health concerns due to its persistence and bioaccumulation. While CPF-induced toxicity in multiple organ systems has been documented, its long-term impact on thyroid homeostasis and the underlying mechanisms remain poorly understood. This study aimed to investigate the subchronic effects of CPF on thyroid function and elucidate the underlying mechanisms of CPF-induced thyroid toxicity.Methods The study utilized 4-week-old male C57BL/6J mice as experimental subjects. These mice were exposed to CPF via intragastric gavage at doses of 3 or 6 mg/kg for a duration of 8 weeks. Throughout the study period, various parameters were assessed, including body weight, serum antioxidant capacity, thyroid endocrine function and structure, apoptosis markers, inflammatory cytokines, and relevant molecular pathways.Results The study revealed that CPF exposure resulted in significant systemic toxicity, manifested through reduced body weight and impaired serum antioxidant capacity. Examination of thyroid-specific effects showed disrupted thyroid endocrine function and structure, accompanied by increased apoptosis and elevated inflammatory cytokines. At the molecular level, CPF significantly stimulated thyroid follicle cell pyroptosis by upregulating the expression of Nlrp3, Caspase-1, and Gsdmd. Further mechanistic analysis demonstrated that CPF activated thyroid follicular cell pyroptosis by modulating the Nrf2/Keap1 antioxidative pathway and enhancing phosphorylation of p65 via NF-κB signaling.Conclusion This comprehensive investigation provides novel insights into the mechanisms of CPF-induced thyroid toxicity. The findings demonstrate that CPF exposure compromises thyroid homeostasis through the induction of follicular cell pyroptosis and modulation of the Nrf2/Keap1/NF-κB signaling axis, highlighting the potential health risks associated with CPF exposure and its impact on thyroid function.
研究领域:
毒理学
·
内分泌学
·
分子生物学
·
环境卫生
·
药理学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Oxidative Medicine and Cellular Longevity
·
2020
·
IF 5.076
Ran Xue,Ming Du,Tian-Yi Zhou,Wan-Zheng Ai,Zhong-Shan Zhang,Xing-Wei Xiang,Yu-Fang Zhou,Zheng-Shun Wen
Hemp seed has been used as a traditional oriental medicine and health food in China for centuries. Polysaccharides from hemp seed (HSP) exhibit important properties of intestinal protection, but there are limited data on the specific underlying mechanism. The primary objective of this study was to investigate the protective effect of HSP on intestinal oxidative damage induced by cyclophosphamide (Cy) in mice. The results showed that pretreatment with HSP significantly increased the average daily gain, thymus index, spleen index, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activity in serum and ileal homogenate and significantly reduced malondialdehyde (MDA) content in ileal homogenate. In addition, the expression levels of SOD, GSH-Px, Nrf2, heme oxidase-1 (HO-1), and quinoneoxidoreductase-1 (NQO1) mRNA in ileal homogenate were significantly increased. Western blot results showed that HSP significantly upregulated the expression of Nrf2 protein and downregulated the expression of Keap1 protein in the ileum. Collectively, our findings indicated that HSP had protective effects on intestinal oxidative damage induced by Cy in mice, and its mechanism might be related to the activation of Nrf2-Keap1 signaling pathway.
研究领域:
药理学
·
毒理学
·
分子生物学
·
营养学
·
动物科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）