Xiongyan Mao, Xiongfei Jing, Songchun Liu, Yuchan Zhou, Li Li, Chen Gu, Xiaohua Wang
{"title":"桑根酚L抑制HMGB1/TLR4/NF-κB信号通路预防脑缺血再灌注损伤。","authors":"Xiongyan Mao, Xiongfei Jing, Songchun Liu, Yuchan Zhou, Li Li, Chen Gu, Xiaohua Wang","doi":"10.1007/s10735-025-10472-w","DOIUrl":null,"url":null,"abstract":"<p><p>Cerebral ischemia/reperfusion damage (CI/RI) is a recurring pathogenic process in post-ischemic stroke. Sanggenol L (SL) is a flavonoid of Morus alba root bark, which exhibits anticancer, neuroprotective, anti-inflammatory, and antioxidant properties. The signaling pathways involved underlying mechanisms of SL on CI/RI are not exploited. To examine the action of SL on CI/R-instigated brain injury through the inflammatory network of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and nuclear factor kappa B (NF-κB) in rats was explored. Rats were separated into 5 sets: control, I/R-induced, I/R + Edaravone (ED, 6 mg/kg bw), I/R + SL (10 mg/kg), I/R + SL (20 mg/kg bw). CI/RI was induced by implanting a thread into the middle cerebral artery occlusion (MCAO) model. Cerebral damages were evaluated by using neurological deficit score, brain edema, brain infarct volume, histopathology, apoptosis, and oxidative stress in rats. SL inhibited cytokines, lipid peroxidation, and apoptosis while improving antioxidant status in MCAO rats. Furthermore, SL therapy reduced I/R-induced brain dysfunction and neuroinflammation by suppressing the HMGB1/TLR4/NF-κB pathways. SL could be a potential strong inhibitor of the CI/RI by suppression of the HMGB1/TLR4/NF-κB signaling pathway. SL's potential anti-inflammatory and antioxidant properties suggest it may be a promising therapeutic agent for CI/RI.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 4","pages":"199"},"PeriodicalIF":2.9000,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Sanggenol L inhibits the HMGB1/TLR4/NF-κB signaling pathway to prevent cerebral ischemia-reperfusion damage.\",\"authors\":\"Xiongyan Mao, Xiongfei Jing, Songchun Liu, Yuchan Zhou, Li Li, Chen Gu, Xiaohua Wang\",\"doi\":\"10.1007/s10735-025-10472-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Cerebral ischemia/reperfusion damage (CI/RI) is a recurring pathogenic process in post-ischemic stroke. Sanggenol L (SL) is a flavonoid of Morus alba root bark, which exhibits anticancer, neuroprotective, anti-inflammatory, and antioxidant properties. The signaling pathways involved underlying mechanisms of SL on CI/RI are not exploited. To examine the action of SL on CI/R-instigated brain injury through the inflammatory network of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and nuclear factor kappa B (NF-κB) in rats was explored. Rats were separated into 5 sets: control, I/R-induced, I/R + Edaravone (ED, 6 mg/kg bw), I/R + SL (10 mg/kg), I/R + SL (20 mg/kg bw). CI/RI was induced by implanting a thread into the middle cerebral artery occlusion (MCAO) model. Cerebral damages were evaluated by using neurological deficit score, brain edema, brain infarct volume, histopathology, apoptosis, and oxidative stress in rats. SL inhibited cytokines, lipid peroxidation, and apoptosis while improving antioxidant status in MCAO rats. Furthermore, SL therapy reduced I/R-induced brain dysfunction and neuroinflammation by suppressing the HMGB1/TLR4/NF-κB pathways. SL could be a potential strong inhibitor of the CI/RI by suppression of the HMGB1/TLR4/NF-κB signaling pathway. SL's potential anti-inflammatory and antioxidant properties suggest it may be a promising therapeutic agent for CI/RI.</p>\",\"PeriodicalId\":650,\"journal\":{\"name\":\"Journal of Molecular Histology\",\"volume\":\"56 4\",\"pages\":\"199\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-06-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Molecular Histology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1007/s10735-025-10472-w\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Molecular Histology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10735-025-10472-w","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Sanggenol L inhibits the HMGB1/TLR4/NF-κB signaling pathway to prevent cerebral ischemia-reperfusion damage.
Cerebral ischemia/reperfusion damage (CI/RI) is a recurring pathogenic process in post-ischemic stroke. Sanggenol L (SL) is a flavonoid of Morus alba root bark, which exhibits anticancer, neuroprotective, anti-inflammatory, and antioxidant properties. The signaling pathways involved underlying mechanisms of SL on CI/RI are not exploited. To examine the action of SL on CI/R-instigated brain injury through the inflammatory network of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and nuclear factor kappa B (NF-κB) in rats was explored. Rats were separated into 5 sets: control, I/R-induced, I/R + Edaravone (ED, 6 mg/kg bw), I/R + SL (10 mg/kg), I/R + SL (20 mg/kg bw). CI/RI was induced by implanting a thread into the middle cerebral artery occlusion (MCAO) model. Cerebral damages were evaluated by using neurological deficit score, brain edema, brain infarct volume, histopathology, apoptosis, and oxidative stress in rats. SL inhibited cytokines, lipid peroxidation, and apoptosis while improving antioxidant status in MCAO rats. Furthermore, SL therapy reduced I/R-induced brain dysfunction and neuroinflammation by suppressing the HMGB1/TLR4/NF-κB pathways. SL could be a potential strong inhibitor of the CI/RI by suppression of the HMGB1/TLR4/NF-κB signaling pathway. SL's potential anti-inflammatory and antioxidant properties suggest it may be a promising therapeutic agent for CI/RI.
期刊介绍:
The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes.
Major research themes of particular interest include:
- Cell-Cell and Cell-Matrix Interactions;
- Connective Tissues;
- Development and Disease;
- Neuroscience.
Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance.
The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.