INTERNATIONAL IMMUNOPHARMACOLOGY
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2023
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IF 5.6
Jingchao Qiang,Rongrong Yang,Xueqing Li,Xuhui Xu,Mengyuan Zhou,Xiaomeng Ji,Yingzhi Lu,Zibo Dong
Sepsis is a systemic inflammatory disease that is caused by a dysregulated host response to infection and is a life-threatening organ dysfunction that affects many organs, which includes the colon. Mounting evidence suggests that sepsis-induced colonic damage is a major contributor to organ failure and cellular dysfunction. Monotropein (MON) is the major natural compound in the iris glycoside that is extracted from Morendae officinalis radix , which possesses the potent pharmacological activities of anti-inflammatory and antioxidant properties. This research evaluated whether MON is able to alleviate septic colonic injury in mice by cecal ligation and puncture. Colonic tissues were analyzed using histopathology, immunofluorescence, quantitative real-time polymerase chain reaction, and Western blot methods. It was initially discovered that MON reduced colonic damage in infected mice, in addition to inflammation, apoptosis, and oxidative stress in colonic tissues, while it activated autophagy, with the NRF2/keap1 and PINK1/Parkin pathways also being activated. Through the stimulation of NCM460 cells with lipopolysaccharides, an in vitro model of sepsis was created as a means of further elucidating the potential mechanisms of MON. In the in vitro model, it was found that MON could still activate the NRF2/keap1, PINK1/Parkin, and autophagy pathways. However, when MON was paired with the NRF2 inhibitor ML385, it counteracted MON-induced activation of PINK1/Parkin and autophagy, while also promoting inflammatory response and apoptosis in NCM460 cells. Therefore, the data implies that MON could play a therapeutic role through the activation of the NFR2/PINK pathway as a means of inducing autophagy to alleviate the oxidative stress in colonic tissues that is induced by sepsis, which will improve inflammation and apoptosis in colonic tissues.
研究领域:
药理学
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免疫学
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分子生物学
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病理学
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DOI
PubMed
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
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2025
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IF 3.3
Xiaoyu Wu,Chuanbo Ding,Xinglong Liu,Qiteng Ding,Shuai Zhang,Yue Wang,Ting Zhao,Wencong Liu
Carotid atherosclerosis (CAS) is a complex cardiovascular disease linked to inflammatory response and oxidative stress. This study aimed to develop and assess the therapeutic efficacy of Phlorizin liposomes (Phlorizin-Lips) in repairing CAS in rats. Phlorizin-Lips were prepared using the film dispersion method and evaluated for controlled release, antioxidant properties, and biocompatibility. The methodology included preparing Phlorizin-Lips, conducting in vitro and in vivo experiments, observing histopathological changes in carotid arteries in a rat model, and detecting inflammatory markers and antioxidant gene expression in arterial endothelial cells using immunoblotting and ELISA. Results showed that Phlorizin-Lips significantly lowered inflammatory markers TNF-α and IL-1β in endothelial cells while upregulating Nrf2 and its downstream antioxidant genes, enhancing the cells' antioxidant capacity and reducing oxidative damage by activating the Nrf2 signaling pathway. Additionally, Phlorizin-Lips reduced carotid plaque formation, improved vascular endothelial function, and promoted CAS repair. This study underscores Phlorizin's potential as a therapeutic agent for CAS and highlights the Nrf2 pathway's role in regulating inflammation and oxidative stress. Future research will explore the clinical potential of Phlorizin-Lips.
研究领域:
药理学
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心血管病学
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分子生物学
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DOI
PubMed
高影响因子
Journal of Functional Foods
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2021
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IF 4.451
Xiang-Rong Cheng,Piao-Han Tu,Wen-Le Dong,Bu-Tao Yu,Shu-Fang Xia,Mitchell N. Muskat,Bin Guan
Xiaoheiyao , the rhizomes of Inula nervosa Wall., is a culinary spice known to contain some electrophilic Nrf2 activators that could potentially intervene in nonalcoholic fatty liver disease (NAFLD). In this study, the electrophilic components from Xiaoheiyao were annotated by comprehensive cheminformatics analyses on UHPLC-MS/MS data after being knocked out with glutathione (GSH)-immobilized magnetic microspheres. Their intervention effects against hepatic steatosis were investigated in free fatty acid (FFA)-treated HepG2 cells. The electrophilic components in Xiaoheiyao were found to be the major bioactive components preventing hepatic steatosis in FFA-treated HepG2 cells. In particular, 10-isobutyryloxy-8,9-epoxythymol isobutyrate (XHY-1) improved hepatic lipid metabolism disorder, Krebs cycle activity, oxidative phosphorylation, and the cellular and mitochondrial redox status. Moreover, XHY-1 activates the Nrf2-ARE signaling pathway through the up-regulation of Nrf2 expression and promotion of Nrf2 nuclear translocation. Molecular docking further showed that XHY-1 could conjugate with Cys151 in the BTB domain of Keap1 through the epoxy group. In conclusion, the electrophilic components of Xiaoheiyao , especially XHY-1, attenuated hepatic steatosis in FFA-treated HepG2 cells through activation of the Nrf2-ARE signaling pathway.
研究领域:
药理学
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细胞生物学
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分子生物学
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药物化学
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产品关联
DOI
高影响因子
PHYTOMEDICINE
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2022
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IF 6.656
Qianqian Jiang,Xu Chen,Xue Tian,Jingmei Zhang,Siming Xue,Yanyan Jiang,Tiantian Liu,Xiaoping Wang,Qianbin Sun,Yiqin Hong,Chun Li,Dongqing Guo,Yong Wang,Qiyan Wang
Background Doxorubicin (DOX) is a powerful anti-tumor anthracycline drug . However, its clinical use is limited due to the side effect of cardiotoxicity . Tanshinone I (Tan I) is one of the major tanshinones isolated from Salvia miltiorrhiza . Studies have shown that Tan I is effective in the treatment of cardiovascular diseases. However, the potential effects of Tan I against DOX-induced cardiotoxicity (DIC) have yet to be explored. Purpose This study aimed to explore whether Tan I can protect against DIC and to reveal whether Tan I can exert anti-oxidative effect by regulating nuclear erythroid factor 2-related factor 2 (Nrf2) pathway. Methods DIC models were established in vivo by intravenous injection of DOX. Echocardiography was used to monitor the cardiac function of mice. Transmission electron microscopy was used to assess mitochondrial damage. Oxidative stress was measured by dihydroethidium (DHE) staining and western blotting . The accumulation and nuclear translocation of Nrf2 was detected by immunofluorescence. H9C2 cellular DIC model was established in vitro to explore the pharmacological mechanism. Nrf2 small interfering (si)-RNA was applied to H9C2 cells to explore whether Tan I exerted protective effect against DIC through Nrf2 signaling pathway . The protective effects of Tan I on mitochondrial function and mitochondrial membrane permeability were measured by MitoSOX™ Red and JC-1 staining assays, respectively. Results In vivo experiments revealed that Tan I could improve cardiac function and protect against DOX-induced myocardial structural damages in mice models. The oxidative stress induced by DOX was suppressed and apoptosis was mitigated by Tan I treatment. Tan I protected against DOX-induced mitochondrial structural damage. Meanwhile, key proteins in Nrf2 pathways were upregulated by Tan I treatment. In vitro studies showed that Tan I attenuated DOX-induced generation of reactive oxygen species (ROS) in cultured H9C2 cells, reduced apoptotic rates , protected mitochondrial functions and up-regulated Nrf2 signaling pathway. Tan I promoted accumulation and nuclear translocation of Nrf2 protein. In addition, interference of Nrf2 abrogated the anti-oxidative effects of Tan I and reversed the expressions of key proteins in Nrf2 pathway. The protective effects of Tan I on mitochondrial integrity was also mitigated by Nrf2 interference. Conclusion Tan I could reduce oxidative stress and protect against DIC through regulating Nrf2 signaling pathway. Nrf2 is a potential target and Tan I is a novel candidate agent for the treatment of DIC.
研究领域:
药理学
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心血管疾病
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
CANCER RESEARCH
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2025
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IF 16.6
Zhou Hai-Meng,Liu Yi,Shi Feng,Qiu Hao-Wen,Li Le,Shu Qi-Peng,Liu Yu-Ying,Wang Bai-Qi,Gao Meng,Du Run-Lei,Ke Shao-Bo,Zhang Xiao-Dong
Ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, plays a crucial role in colorectal cancer (CRC) progression and therapeutic response. The NRF2 pathway is one of the critical axes in ferroptosis regulation, which governs oxidative stress resistance and iron homeostasis through its downstream targets, including HMOX1, SLC7A11, and others. However, HMOX1 and SLC7A11 exhibit contrasting roles in ferroptosis, with HMOX1 promoting ferroptosis via iron accumulation and lipid peroxidation, while SLC7A11 inhibits ferroptosis by enhancing antioxidant defenses. Here, we identified CLK2 as a key regulator of the delicate balance of the opposing effects of HMOX1 and SLC7A11. CLK2 stabilized KEAP1 to suppress NRF2 activity, resulting in the downregulation of HMOX1 and SLC7A11. Simultaneously, CLK2 downregulated p53, thereby relieving p53-mediated repression of SLC7A11. The dual regulation by CLK2 disrupted the balance between HMOX1 and SLC7A11, leading to excessive activation of HMOX1 in the absence of CLK2, ultimately sensitizing CRC cells to ferroptosis. Additionally, CLK2 promoted CRC proliferation and tumorigenesis in patient-derived organoids, cell lines, and mouse models. Furthermore, combining the ferroptosis inducer Erastin with Oxaliplatin significantly enhanced anti-tumor efficacy in CLK2-deficient xenograft models. Together, this study establishes CLK2 as a critical inhibitor of ferroptosis via the KEAP1/NRF2/HMOX1 and p53/SLC7A11 axes, supporting its potential as a therapeutic target for CRC.
研究领域:
癌症生物学
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分子生物学
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细胞死亡
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信号转导
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肿瘤学
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药理学
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产品关联
DOI
PubMed
高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
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2025
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IF 8.2
Hailin Wang,Yueying Wang,Xin Li,Jiayang Ma,Zhiqi Hu,Qian Qu,Yong Miao
Hair graying and loss are significant indicators of aging, and oxidative stress plays an essential role in this progression. Ergothioneine (EGT), potent antioxidant from edible fungi and certain prokaryotes, regulates the antioxidant defense system. However, its anti-aging effects on hair follicles (HFs) are remain obscure. We used dermal papilla cells (DPCs) co-culture system, HFs organ culture system, aged mice and H 2 O 2 -induced gray hair mice to explore the antioxidative functions and mechanisms of EGT on HFs. Research demonstrated that EGT mitigated H 2 O 2 -induced DPCs damage, reduced the secretion of inflammatory factors (IL-6, IL-1β, and TNF-α) and enhanced the production of pigmentation promoting factors (SCF and SDF1) through the SIRT1/Nrf2 pathway in DPCs. In vitro experiments of co-culture system indicated that EGT-treated DPCs remarkably alleviated oxidative damages and promoted cell proliferation in A-375 and HaCaT. Furthermore, it increased tyrosinase activity, melanin content and the expression of key melanin synthesis genes in A-375. Meanwhile, it promoted the expression of K19 and K14 in HaCaT. In vivo experiments revealed that EGT exhibited excellent effects on reducing pigmentation disfunction and hair loss in aged mice and H 2 O 2 -induced gray hair mice. In the HFs organ culture, the EGT promoted hair growth and pigmentation via SIRT1/Nrf2 partly. Our research indicated that EGT had potent antioxidant and anti-aging functions for HFs. This not only provided new applications for EGT but also opened up new therapeutic avenues for hair aging.
研究领域:
细胞生物学
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医学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
BIOMEDICAL AND ENVIRONMENTAL SCIENCES
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2025
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IF 4.1
Jia Lin Liu,Min Wang,Rui Zhang,Ji Fang Zheng,Xi Xiu Jiang,Qiao Ni Hu
Objective: To explore the protective effects and underlying mechanisms of H 2 S against lipid peroxidation-mediated carbonyl stress in the uranium-treated NRK-52E cells. Methods: Cell viability was evaluated using CCK-8 assay. Apoptosis was measured using flow cytometry. Reagent kits were used to detect carbonyl stress markers malondialdehyde, 4-hydroxynonenal, thiobarbituric acid reactive substances, and protein carbonylation. Aldehyde-protein adduct formation and alcohol dehydrogenase, aldehyde dehydrogenase 2, aldo-keto reductase, nuclear factor E2-related factor 2 (Nrf2), and cystathionine β-synthase (CBS) expression were determined using western blotting or real-time PCR. Sulforaphane (SFP) was used to activate Nrf2. RNA interference was used to inhibit CBS expression. Results: GYY4137 (an H 2 S donor) pretreatment significantly reversed the uranium-induced increase in carbonyl stress markers and aldehyde-protein adducts. GYY4137 effectively restored the uranium-decreased Nrf2 expression, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2, accompanied by a reversal of the uranium-decreased expression of CBS and aldehyde-metabolizing enzymes. The application of CBS siRNA efficiently abrogated the SFP-enhanced effects on the expression of CBS, Nrf2 activation, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2 and concomitantly reversed the SFP-enhanced effects of the uranium-induced mRNA expression of aldehyde-metabolizing enzymes. Simultaneously, CBS siRNA reversed the SFP-mediated alleviation of the uranium-induced increase in reactive aldehyde levels, apoptosis rates, and uranium-induced cell viability. Conclusion: H 2 S induces Nrf2 activation and nuclear translocation, which modulates the expression of aldehyde-metabolizing enzymes and the CBS/H 2 S axis. Simultaneously, the Nrf2-controlled CBS/H 2 S axis may at least partially promote Nrf2 activation and nuclear translocation. These events form a cycle-regulating mode through which H 2 S attenuates the carbonyl stress-mediated NRK-52E cytotoxicity triggered by uranium.
研究领域:
毒理学
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Materials Today Bio
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2025
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IF 10.2
Qiang Zhang,Tuo Wang,Junyu Ren,Yanru Guo,Ziyi Yin,Chenrui Zhang,Honglin Fan,Yinting Ren,Junlong Da,Narisu Hu
Oral ulcers, a prevalent mucosal disorder with high recurrence rates, remain challenging to treat due to the oral cavity’s dynamic environment and the multifactorial nature of ulcer progression. Here, we report a multifunctional microneedle (MN) patch loaded with astragalus polysaccharide (APS-MN) that integrates rapid mucosal penetration, reactive oxygen species (ROS) scavenging, and ferroptosis inhibition to accelerate ulcer healing. Unlike conventional MN systems reliant on synthetic drugs or prolonged dissolution, APS-MN leverages the natural antioxidant and immunomodulatory properties of APS-a traditional Chinese medicine-derived polysaccharide-enabling complete drug release within 2 minutes and targeted delivery to ulcer bases. In vitro and in vivo studies demonstrate that APS-MN promotes M2 macrophage polarization, suppresses pro-inflammatory cytokines (TNF-α, IL-1β), and inhibits ferroptosis via the Nrf2/HO-1/SLC7A11 axis, achieving 88.2% wound closure in rats within 6 days. Notably, this work combined herbal polysaccharides with MN technology for oral ulcer therapy, offering a biocompatible, non-invasive alternative to corticosteroids and antibiotics. The rapid dissolution, dual antioxidant/anti-ferroptotic action, and scalability of APS-MN position it as a transformative platform for managing recurrent oral ulcers and other redox-imbalanced mucosal diseases.
研究领域:
药学
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生物医学工程
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免疫学
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产品关联
DOI
PubMed
高影响因子
POULTRY SCIENCE
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2024
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IF 3.8
Jiamei Zhu,Xueyan Dai,Yan Wang,Ting Cui,Bingyan Huang,Dianyun Wang,Wenjing Pu,Caiying Zhang
Cadmium ( Cd ) and high molybdenum ( Mo ) are injurious to the body. Previous research has substantiated that Cd and Mo exposure caused testicular injury of ducks, but concrete mechanism is not fully clarified. To further survey the toxicity of co-exposure to Cd and Mo in testis, 40 healthy 8-day-old Shaoxing ducks ( Anas platyrhyncha ) were stochasticly distributed to four groups and raised with basic diet embracing Cd (4 mg/kg Cd) or Mo (100 mg/kg Mo) or both. At the 16th week, testis tissues were gathered. The characteristic ultrastructural changes related to apoptosis and ferroptosis were observed in Mo or Cd or both groups. Besides, Mo or Cd or both repressed nuclear factor erythroid 2-related factor 2( Nrf2 ) pathway via decreasing Nrf2, Heme oxygenase-1 ( HO-1 ), NAD(P)H quinone oxidoreductase 1 ( NQO1 ), Glutamate-cysteine ligase catalytic subunit ( GCLC ) and Glutamate-cysteine ligase modifier subunit ( GCLM ) mRNA expression of and Nrf2 protein expression, then stimulated apoptosis by elevating Bcl-2 antagonist/killer-1 ( Bak-1 ), Bcl-2-associated X-protein ( Bax ), Cytochrome complex ( Cyt-C ), caspase-3 mRNA expression, cleaved-caspase-3 protein expression and apoptosis rate, as well as reducing B-cell lymphoma-2 ( Bcl-2 ) mRNA expression and ratio of Bcl-2 to Bax, and triggered ferroptosis by upregulating Acyl-CoA Synthetase Long Chain Family Member 4 ( ACSL4 ), transferrin receptor ( TFR1 ) and Prostaglandin-Endoperoxide Synthase 2 ( PTGS2 ) expression levels, and downregulating ferritin heavy chain 1 ( FTH1 ), ferritin light chain 1 ( FTL1 ), ferroportin 1 ( FPN1 ), solute carrier family 7 member 11 ( SCL7A11 ) and glutathione peroxidase 4 ( GPX4 ) expression levels. The most obvious changes of these indexes were observed in co-treated group. Altogether, the results announced that Mo or Cd or both evoked apoptosis and ferroptosis by inhibiting Nrf2 pathway in the testis of ducks, and co-exposure to Mo and Cd exacerbated these variations.
研究领域:
毒理学
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生殖生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
MOLECULES
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2022
·Vol. 27
·期 12
·3823
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IF 4.927
Meng Zhou,Yanpeng Dai,Yong Ma,Yi Yan,Min Hua,Qi Gao,Xue Geng,Qian Zhou
Acute kidney injury (AKI) induced by cisplatin (CP), a first-line anticancer drug for chemotherapy, is common. To date, there is an urgent need to find effective treatments to reduce the nephrotoxicity caused by CP. Meanwhile, the restoration of mitochondrial dysfunction shows potential to be used as an adjunct to conventional therapeutic strategies. This study found that liquiritigenin can ameliorate mitochondrial dysfunction and acute kidney injury induced by CP in mice. The intraperitoneal injection of 15 mg/kg body weight liquiritigenin for 2 days markedly protected against CP-induced mitochondrial dysfunction, restored renal tubule and mitochondrial morphology, decreased blood Scr and BUN levels, and decreased cell apoptosis. Furthermore, the elevated expression of SIRT3 induced by liquiritigenin, which can be upregulated by NRF2, was confirmed in vivo and in vitro. The underlying protective mechanisms of liquiritigenin in CP-induced nephrotoxicity were then investigated. Molecular docking results showed that liquiritigenin has potent binding activities to KEAP1, GSK-3β and HRD1. Further results showed that liquiritigenin induced the nuclear translocation of NRF2 and increased the levels of mitochondrial bioenergetics-related protein such as PGC-1α, and TFAM, which are related to NRF2 activity and mitochondrial biogenesis. In addition, liquiritigenin was found to possibly reverse the decrease in BCL2/BAX ratio induced by CP in live cultured renal tubule epithelial cells. Collectively, these results indicated that liquiritigenin could be used as a potential nephroprotective agent to protect against cisplatin-induced acute kidney injury in a NRF2-dependent manner by improving mitochondria function.Keywords:liquiritigenin;NRF2;cisplatin;SIRT3;mitochondrial biogenesis
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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肾脏生理学
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DOI
PubMed
高影响因子
BMC Cardiovascular Disorders
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2024
·Vol. 24
·期 1
·1-12
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IF 2
Qian Kai,Song Li,Guo Jia-Min,Fu Dan,Shi Jia,Ma Yu,Ge Zi-Jie,Li Lei,Zhang Su-qin
Background Cardiovascular disease carries the highest mortality rate among diseases, and pharmacological interventions have limited efficacy. Baicalin (Bai) promotes biological metabolic processes, eliminates oxygen free radicals, and is anti-inflammatory. This study aimed to investigate the effect of Bai on the cardiac injury model induced by isoproterenol in mice.Methods and ResultIn this study, all groups except the control received intraperitoneal injections of isoproterenol (ISO) to induce a cardiac injury model, with the drug administered continuously for 14 days. hematoxylin and eosin staining and Masson’s trichrome staining revealed that Bai significantly mitigated ISO-induced pathological changes in mouse heart tissue and alleviated myocardial hypertrophy. Echocardiography assessments demonstrated that Bai preserved cardiac function in ISO-treated mice. Furthermore, our findings indicated that Bai activated the Nrf2 signaling pathway in vivo and in vitro. To delve deeper, mice were further treated with ML385 (ML) via intraperitoneal injection to inhibit the Nrf2 pathway. Results showed that ML385 blocked the cardioprotective effects of Bai in mouse heart tissue.Conclusion Bai protects against ISO-induced cardiac injury, and its mechanism is related to activating the Nrf2/HO-1 signaling pathway to regulate cardiac ferroptosis and improve cardiac remodeling.
研究领域:
心血管疾病
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药理学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Genes
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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
研究领域:
血液学
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分子生物学
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细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
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