JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
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2025
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IF 3.5
Yan-Xia Li,He Ma,Le Shi,Zhong-Fei Zhang,Yu-Meng Wu,Chao Yan,Yan Chen,Yong-Ming Lu
BACKGROUND Polysaccharides from Pleurotus citrinopileatus exhibit diverse bioactivities, yet their efficacy against ultraviolet B (UVB)-induced photoaging remains unexplored. This study aimed to purify and characterize a specific PCP and assess its protective effects using a UVB-induced zebrafish model. RESULTS A polysaccharide, designated as PCP-2, was isolated from P. citrinopileatus through hot-water extraction, ultrafiltration and chromatography. PCP-2 is a galactoglucan with a molecular weight of 1.52 × 10 6 Da, predominantly composed of 1,4-linked glucopyranosyl and 1,4,6-linked galactopyranosyl residues. In UVB-exposed zebrafish, PCP-2 administration resulted in a significant reduction of reactive oxygen species and malondialdehyde levels, alongside enhanced activities of antioxidant enzymes, including superoxide dismutase, catalase and glutathione peroxidase. Additionally, PCP-2 inhibited apoptosis by upregulating Bcl-2 expression and downregulating caspase-3. It also attenuated cellular senescence, as indicated by decreased β -galactosidase activity and increased telomerase activity. Moreover, PCP-2 promoted the synthesis of type I and III collagen by suppressing matrix metalloproteinases MMP-1 and MMP-3 and reduced melanin production through the downregulation of tyrosinase expression. Mechanistic studies suggested that these protective effects are mediated via activation of the Nrf2/HO-1 signaling pathway. CONCLUSION PCP-2 from P. citrinopileatus effectively mitigates UVB-induced photoaging, primarily by activating the Nrf2/HO-1 pathway. These findings suggest PCP-2's potential as an anti-photoaging agent in both food and pharmaceutical industries. © 2025 Society of Chemical Industry.
研究领域:
生物化学
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药理学
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食品科学
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产品关联
DOI
PubMed
高影响因子
Scientific Reports
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2025
·Vol. 15
·期 1
·1-12
·
IF 3.9
Cheng Chunfang,Zhang Shasha,Chen Chong,Gong Yanchun,Ding Kaizhi,Li Guoyin,Jiang Wei,Zhang Zhenyu,He Bin,Hu Zhihong,Li Yuhua,Yao Lihua
Excessive exercise can lead to physical fatigue and disruption of the antioxidant system, resulting in neurological damage and cognitive decline. Cordycepin, the main component of Cordyceps militaris , has anti-inflammatory, antioxidant and neuroprotective effects. In this study, the anti-fatigue effect and potential mechanism of action of cordycepin were investigated using a forced exercise mouse model. The results showed that oral administration of cordycepin enhanced exercise endurance, increased liver and muscle glycogen content, and simultaneously decreased serum levels of lactic acid, lactate dehydrogenase, creatine kinase, and blood urea nitrogen ( p < 0.05). In addition, cordycepin had antioxidant effects, increasing superoxide dismutase activity and decreasing serum malondialdehyde (MDA) levels ( p < 0.01). In vitro experiments further demonstrated the antioxidant and anti-fatigue effects of cordycepin. Behavioral tests showed that the learning and memory ability of mice in the excessive exercise model group decreased to 40% compared with the control group. Cordycepin alleviated the learning and memory deficits in the over-exercised mice, significantly reduced the levels of fatigue metabolites and oxidative stress in vivo ( p < 0.05), and altered the levels of neurotransmitters levels ( p < 0.05). Furthermore, cordycepin modulated Keap1/Nrf2/HO-1-mediated oxidative stress and enhanced BDNF levels ( p < 0.05). These findings suggest that cordycepin can alleviate excessive exercise-induced fatigue by modulating the Keap1/Nrf2/HO-1 signaling pathway and BDNF expression, providing strong supporting evidence for the development of cordycepin-functional foods or anti-fatigue drugs.
研究领域:
运动生理学
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药理学
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神经科学
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DOI
PubMed
高影响因子
Antioxidants
·
2023
·Vol. 12
·期 2
·370
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IF 7
Chongshan Dai,Mingchao Liu,Qinzhi Zhang,Subhajit Das Gupta,Shusheng Tang,Jianzhong Shen
Nootkatone (NKT), a major ingredient of Alpinia oxyphylla, exhibited potential nephroprotective effects; however, the precise molecular mechanisms remain poorly understood. This study aimed to study the nephroprotective effects of NKT and the underlying mechanisms in a mouse model. Our results showed that NKT pretreatment at the doses of 5, 10, and 20 mg/kg per day for 7 days significantly attenuates carbon tetrachloride (CCl4)-induced increases of serum BUN and CRE and kidney pathology injury. NKT pretreatment also markedly inhibited oxidative stress, inflammatory response, and the activation of caspases-9 and -3 in kidneys of mice exposed to CCl4. Meanwhile, NKT pretreatment downregulated the expression of NOX4, IL-1β, IL-6, and TNF-α proteins and NO levels in the kidney tissues. Moreover, NKT pretreatment upregulated the expression of Nrf2 and HO-1 mRNAs, and downregulated the expression of NF-κB, IL-1β, IL-6, TNF-α, and iNOS mRNAs in the kidneys of mice, compared to those in the CCl4alone treatment group. In conclusion, our results reveal that NKT supplementation could protect against CCl4exposure-induced oxidative stress and inflammatory response in the kidneys by inhibiting NOX4 and NF-κB pathways and activating the Nrf2/HO-1 pathway. Our current study highlights the therapeutic application of NKT for kidney diseases.Keywords:nootkatone;oxidative stress;nephrotoxicity;Nrf2/HO-1 pathway;NF-κB pathway
研究领域:
药理学
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毒理学
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分子生物学
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
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2025
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IF 4.7
Ji-Ping Wei,Bo Zhao,Zi-Jian Jiang,Peng-Yu Wang,Yan Xu,Ning Ding,Yuan-Yuan Hu,Wei Wang,Bo-Tao Jiang
Renal ischemia/reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). It can progress to chronic injury and subsequently to chronic kidney disease (CKD) via the renal fibrosis pathway. Luteolin is one of the most commonly occurring flavonoids and exhibits potential therapeutic activity against various pathophysiological processes. In this study, we investigated the protective role of luteolin in counteracting renal I/R injury and its potential mechanisms through systematic network pharmacology, molecular docking, and in vivo experimental studies. Using network pharmacology, we constructed and analyzed a luteolin-renal I/R injury target network. We assessed the relationship between luteolin and renal I/R injury targets using molecular docking analysis. Subsequently, we established a rat model of AKI to CKD transition using unilateral ischemia/reperfusion injury (UIRI), and detected changes in the expression of related proteins using biochemical indices. Network pharmacological analysis and molecular docking showed that luteolin affected renal I/R injury through multiple targets and pathways. As demonstrated by in vivo experiments, luteolin significantly attenuated renal I/R-induced oxidative injury by inhibiting renal lipid peroxidation in rats through the modulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. Luteolin attenuated the levels of relevant inflammatory markers, significantly upregulated the synthesis of apoptosis-related proteins, and downregulated the expression of anti-apoptotic proteins. Our results suggest that luteolin effectively inhibited oxidative damage, inflammation, apoptosis, and fibrosis caused by renal I/R injury, thus exerting a nephroprotective effect. The antioxidant effects of luteolin may be related to the regulation of Nrf2/HO-1 signaling.
研究领域:
药理学
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分子生物学
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肾脏病学
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产品关联
DOI
PubMed
高影响因子
MOLECULES
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2018
·Vol. 23
·期 1
·215
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IF 3.098
Xinyan Peng,Chongshan Dai,Quanwen Liu,Junke Li,Jingru Qiu
This study aimed to investigate the protective effect of curcumin against carbon tetrachloride (CCl4)-induced acute liver injury in a mouse model, and to explain the underlying mechanism. Curcumin at doses of 50, 100 and 200 mg/kg/day were administered orally once daily for seven days prior to CCl4exposure. At 24 h, curcumin-attenuated CCl4induced elevated serum transaminase activities and histopathological damage in the mouse’s liver. Curcumin pre-treatment at 50, 100 and 200 mg/kg significantly ameliorated CCl4-induced oxidative stress, characterized by decreased malondialdehyde (MDA) formations, and increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) content, followed by a decrease in caspase-9 and -3 activities. Curcumin pre-treatment significantly decreased CCl4-induced inflammation. Furthermore, curcumin pre-treatment significantly down-regulated the expression of TGF-β1 and Smad3 mRNAs (bothp< 0.01), and up-regulated the expression of nuclear-factor erythroid 2-related factor 2 (Nrf2) and HO-1 mRNA (bothp< 0.01) in the liver. Inhibition of HO-1 attenuated the protective effect of curcumin on CCl4-induced acute liver injury. Given these outcomes, curcumin could protect against CCl4-induced acute liver injury by inhibiting oxidative stress and inflammation, which may partly involve the activation of Nrf2/HO-1 and inhibition of TGF-β1/Smad3 pathways.Keywords:curcumin;acute liver injury;Nrf2/HO-1 pathway;oxidative stress;TGF-β1/Smad3 pathway
研究领域:
药理学
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肝病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2016
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IF 3.584
Chongshan Dai,Bin Li,Yan Zhou,Daowen Li,Shen Zhang,Hui Li,Xilong Xiao,Shusheng Tang
The potential toxicity of quinocetone (QCT) has raised widely concern, but its mechanism is still unclear. This study aimed to investigate the protective effect of curcumin on QCT induced apoptosis and the underlying mechanism in human hepatocyte L02 cells. The results showed that QCT treatment significantly decreased the cell viability of L02 cell and increased the release of lactate dehydrogenase (LDH), which was attenuated by curcumin pre-treatment at 1.25, 2.5 and 5 μM. Compared to the QCT alone group, curcumin pre-treatment significantly attenuated QCT induced oxidative stress , mitochondrial dysfunction and apoptosis. In addition, curcumin pretreatment markedly attenuated QCT-induced increase of iNOS activity and NO production in a dose-dependent manner. Meanwhile, curcumin pretreatment markedly down-regulated the expression of nuclear factor –kB (NF-kB) and iNOS mRNAs, but up-regulated the expressions of Nrf2 and HO-1 mRNAs, compared to the QCT alone group. Zinc protoporphyrin IX , a HO-1 inhibitor, markedly partly abolished the cytoprotective effect of curcumin against QCT-induced caspase activation, NF-kB mRNA expression. These results indicate that curcumin could effectively inhibit QCT induced apoptosis and inflammatory response in L02 cells, which may involve the activation of Nrf2/HO-1 and inhibition of NF-kB pathway.
研究领域:
药理学
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毒理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
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2022
·
IF 5.988
Qian Wang,Xiaoyan Yang,Changwei Zhu,Guodong Liu,Weili Han,Yujun Sun,Lisheng Qian
Benincasa hispida Cogn. ( B. hispida ) is a popular vegetable in China, and studies have been reported on B. hispida polysaccharides (BPS) preparation. However, few studies have been reported on its physicochemical and skincare properties. In this study, we analyzed the physicochemical properties of BPS, free radical scavenging capability, moisturizing and antioxidant activities in vitro and in vivo , respectively. Our results show that BPS was an inhomogeneous acidic polysaccharide that could scavenge a variety of free radicals. Also, BPS had a good moisturizing and antioxidant capability both in vitro and in vivo . Specifically, BPS could alter some key antioxidant enzyme activities and pro-inflammatory factor levels via activating the NRF2/HO-1 pathway, thereby preventing H 2 O 2 -induced reactive oxygen species (ROS) production and apoptosis of HDF-1 cells. Our results suggest that BPS exhibited favorable moisturizing and anti-aging properties and might be an attractive candidate for the development of anti-aging skincare products.
研究领域:
药学
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化妆品科学
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生物化学
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药理学
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产品关联
DOI
PubMed
高影响因子
Antioxidants
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2022
·Vol. 11
·期 8
·1498
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IF 7.675
Chongshan Dai,Qinzhi Zhang,Linjie Shen,Gaurav Sharma,Haiyang Jiang,Zhanhui Wang,Jianzhong Shen
Quinocetone (QCT), a member of the quinoxaline 1,4-di-N-oxides (QdNOs) family, can cause genotoxicity and hepatotoxicity, however, the precise molecular mechanisms of QCT are unclear. This present study investigated the protective effect of quercetin on QCT-induced cytotoxicity and the underlying molecular mechanisms in human L02 and HepG2 cells. The results showed that quercetin treatment (at 7.5–30 μM) significantly improved QCT-induced cytotoxicity and oxidative damage in human L02 and HepG2 cells. Meanwhile, quercetin treatment at 30 μM significantly inhibited QCT-induced loss of mitochondrial membrane potential, an increase in the expression of the CytC protein and the Bax/Bcl-2 ratio, and an increase in caspases-9 and -3 activity, and finally improved cell apoptosis. Quercetin pretreatment promoted the expression of the phosphorylation of p38, Nrf2, and HO-1 proteins. Pharmacological inhibition of p38 significantly inhibited quercetin-mediated activation of the Nrf2/HO-1 pathway. Consistently, pharmacological inhibitions of the Nrf2 or p38 pathways both promoted QCT-induced cytotoxicity and partly abolished the protective effects of quercetin. In conclusion, for the first time, our results reveal that quercetin could improve QCT-induced cytotoxicity and apoptosis by activating the p38/Nrf2/HO-1 pathway and inhibiting the ROS/mitochondrial apoptotic pathway. Our study highlights that quercetin may be a promising candidate for preventing QdNOs-induced cytotoxicity in humans or animals.Keywords:quercetin;quinocetone;oxidative stress;apoptosis;p38/Nrf2/HO-1 pathway;NF-κB pathway
研究领域:
毒理学
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细胞生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
Pharmaceuticals
·
2022
·Vol. 15
·期 12
·1548
·
IF 5.215
Fei Yang,Cuizhen Shen
On the basis of the mice pressure ulcers (PU) model, the protective effect and potential mechanism of sodium Danshensu (SDSS) cream against PU were investigated. The mice were randomly divided into three groups: the negative control group (cream without 0.5 g SDSS), the SDSS group (cream containing 0.5 g SDSS), and the positive group (0.5 g Hirudoid®). After 7 and 14 days of ointment application, the wound-healing rate of the SDSS and positive groups was significantly higher than that of the control group (p< 0.05). The results of hematoxylin–eosin staining also indicated that SDSS has the potential to promote the healing of PU. In addition, the serum IL-6, IL-1β, TNF-α, and MDA levels decreased significantly (p< 0.01) after 14 days of SDSS treatment, while the SOD, CAT, and GSH-Px activities increased significantly (p< 0.01). In addition, SDSS cream was able to significantly increase the expression of Nrf2, HO-1, GCLM, NQO1, NF-κB p65, NF-κB p50, IKKα, and IKKβ while decreasing the expression of Keap1 and IκBαin the Nrf2/HO-1 and NF-κB pathways. Our research will provide a foundation for the future clinical prevention and treatment of PU with SDSS cream.Keywords:pressure ulcers;sodium Danshensu cream;ischemia/reperfusion injury;Nrf2/HO-1 pathway;NF-κB pathway
研究领域:
药理学
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伤口愈合
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炎症
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氧化应激
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产品关联
DOI
PubMed
高影响因子
FITOTERAPIA
·
2025
·
IF 2.6
Zongchao Li,Ruoxuan Xu,Can Li,Chenglin Chi,Xiaoli Yang,Shufang Yang,Rongxia Liu
The pericarp of Zanthoxylum bungeanum Maxim. (ZBM) is an edible spice with medicinal value, and it has anti-obesity, anti-inflammatory, and cardiovascular protective effects. This study investigated the therapeutic effect of ZBM on atherosclerosis (AS) and its potential mechanisms. An in vivo experimental model of AS was established on apolipoprotein-E deficient (ApoE −/− ) mice to evaluate the efficacy of ZBM. Serum metabolomics combined with the vascular smooth muscle cell (VSMC) proliferation model were subsequently conducted to analyze the mechanisms. Results showed that ZBM effectively alleviated blood lipid disorders, aortic lipid accumulation, and intimal thickness in mice. Metabolomics indicated that ZBM mainly regulated 5 major metabolic pathways, including TCA cycle, steroid hormone biosynthesis, sphingolipid metabolism, glyoxylate and dicarboxylate metabolism, glycerophospholipid metabolism, which affected lipid metabolism and cell proliferation. Further experiments showed that ZBM inhibited VSMC proliferation likely because it blocked the signal transducer activator of transcription 3 (STAT3) phosphorylation and activated nuclear factor E2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, resulting in G0/G1 phase arrest and reactive oxygen species (ROS) clearance.
研究领域:
药理学
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代谢组学
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心血管疾病
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产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2025
·
IF 4.8
Lili Huang,Yinqi Chen,Hua Zhou,Huihui Chen,Xiping Wu,Zhuochao Wu,Zhoudi Liu,Zhiwei Zheng
Background: Cerebral ischemia-reperfusion injury (CIRI) is a secondary brain injury that occurs after thrombolysis and is a primary cause of death in ischemic stroke patients. Antioxidants that effectively reduce oxidative stress are an efficient treatment approach for CIRI. Here, a novel diimide compound was synthesized using the chemical structure of previously designed anti-inflammatory skeletons.Methods and results: The antioxidant activities of five compounds (Z1–Z5) were preliminarily evaluated using the hydrogen peroxide-induced PC12 cell damage model, of which Z3 exhibited the best antioxidant effect, even exceeding that of the positive control (tert-butylhydroquinone). Enrichment analysis using network targeting and network pharmacology methods predicted seven candidate core target genes of Z3 in CIRI. Of these targets, computer molecular docking analysis predicted that Z3 has the strongest binding affinity for nuclear factor erythroid 2-related factor (Nrf2). MTT and colony formation assays, reactive oxygen species analysis, immunofluorescence, and immunoblotting experiments verified that Z3 reduced reactive oxygen species to play a protective antioxidant role via the Nrf2/hemoxygenase 1 (HO-1) pathway. The protective effect of Z3 in vivo was explored through TTC staining and neurobehavioral scoring of CIRI model mice.Conclusion: This study provides a new drug development strategy and candidate drug for the treatment of CIRI, offering ideas for the design of new antioxidants.
研究领域:
神经科学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Current Nanoscience
·
2024
·Vol. 21
·期 4
·757-765
·
IF 1.4
Zirui Liu,Dan Li,Baofeng Zhao,Xifan Mei
BackgroundGouty arthritis, characterized by excruciating pain and discomfort, poses a significant burden on patients. While nanomedicines have shown promise in addressing this ailment, their complicated synthesis processes often involve potentially toxic procedures, contributing to adverse side effects in disease management.MethodsIn this study, we introduce a straightforward and elegant solution by utilizing easily prepared gold platinum (AuPt) nanoparticles for the treatment of gouty arthritis. The synthesis of these nanoparticles involves the use of gold and platinum precursors in conjunction with NaBH4, simplifying the manufacturing process. Experimental models of gout were established in both in vivo and in vitro settings through lipopolysaccharide and monosodium urate crystal induction.ResultsOur findings revealed that AuPt nanoparticles exhibited potent anti-inflammatory effects against gout. This effect was attributed to their ability to activate the Nrf2/HO-1 pathway, resulting in pain alleviation and the inhibition of inflammation, ultimately leading to the reduction of joint edema. With their uncomplicated synthesis and promising therapeutic potential, these simply prepared AuPt nanoparticles emerge as a compelling candidate for pharmaceutical intervention in the treatment of gouty arthritis.ConclusionThis approach not only holds the promise of delivering effective relief to patients but also minimizes the risk of unwanted side effects associated with complex nanomedicine synthesis processes.
研究领域:
药理学
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纳米医学
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炎症研究
✓ 已验证
DOI
高影响因子
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