| 白藜芦醇抑制NLRP3炎性小体介导的细胞焦亡信号通路改善肥胖小鼠认知功能 |
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| 引用本文： | 董雯,伦永志,刘 奔,孙 杰,潘凌鸿.白藜芦醇抑制NLRP3炎性小体介导的细胞焦亡信号通路改善肥胖小鼠认知功能[J].现代预防医学,2022,0(15):2814-2820. |
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| 作者姓名： | 董雯 伦永志 刘 奔 孙 杰 潘凌鸿 |
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| 作者单位： | 莆田学院药学与医学技术学院医学检验系，医学微生态学福建省高校重点实验室，福建 351100 |
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| 摘 要： | 目的 观察白藜芦醇（RES）对肥胖小鼠认知功能的保护作用，并探讨其海马组织核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎性小体—细胞焦亡信号通路机制。方法 50只小鼠随机均分为:正常对照组、模型组和白藜芦醇高（100mg/kg）、中（50mg/kg）、低（25mg/kg）剂量组，喂养6个月后，检测小鼠认知功能，海马组织细胞焦亡水平，海马组织沉默信息调节因子1（SIRT1）、NLRP3、半胱氨酸天冬氨酸蛋白酶1（Caspase-1）、白细胞介素-1β（IL-1β）、IL-18和肿瘤坏死因子-α（TNF-α）等蛋白表达情况。采用单因素方差分析或重复测量方差分析进行结果分析。结果 与模型组比较，白藜芦醇高剂量组小鼠终体质量降低（t=-14.453，P=0.021），海马组织细胞焦亡水平降低（t=-17.328，P=0.011），学习记忆能力改善，海马组织SIRT1蛋白表达升高（t=32.812，P＜0.001），NLRP3、Caspase-1、IL-1β、IL-18和TNF-α蛋白表达均下降（t=-28.462，P=0.003；t=-38.148，P＜0.001；t=-38.809，P＜0.001；t=-47.239，P＜0.001；t=-48.811，P＜0.001），白藜芦醇低剂量组组小鼠终体质量、海马组织细胞焦亡水平、学习记忆能力均无改善，海马组织SIRT1、NLRP3、Caspase-1、IL-1β、IL-18和TNF-α蛋白表达无统计学差异（t=12.012，P=0.132；t=-14.252，P=0.104；t=-19.219，P=0.083；t=-7.252，P=0.512；t=-15.252，P=0.286；t=-21.252，P=0.068）。结论 RES具有浓度效应，可以改善肥胖及其所致认知功能障碍，其机制可能与促进海马组织SIRT1、抑制NLRP3炎性小体—细胞焦亡信号通路有关。
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| 关 键 词： | 白藜芦醇 SIRT1 NLRP3炎性小体 细胞焦亡 肥胖 |
Resveratrol ameliorated cognitive function of diet- induced obesity mice through inhibiting pyroptosis mediated by NLRP3 inflammasome |
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| DONG Wen,LUN Yong-zhi,LIU Ben,SUN Jie,PAN Ling-hong.Resveratrol ameliorated cognitive function of diet- induced obesity mice through inhibiting pyroptosis mediated by NLRP3 inflammasome[J].Modern Preventive Medicine,2022,0(15):2814-2820. |
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| Authors: | DONG Wen LUN Yong-zhi LIU Ben SUN Jie PAN Ling-hong |
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| Affiliation: | Dept. of Laboratory Medicine, School of Pharmacy and Medical Technology, Putian University, Key Laboratory of Medical Microecology (Putian University), Fujian Province University, Putian, Fujian 351100, China |
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| Abstract: | Objective To explore the effects of resveratrol (RES) on the cognitive capability and the expression of the proteins related to the Nod-like receptor protein 3 (NLRP3) inflammasome-pyroptosis signal pathway in hippocampus of diet- induced obesity mice. Methods 50 mice were randomly divided into 5 groups (n=10): normal diet group (CON group), high-calorie diet group (HCD group), HCD+100 mg/kg RES group (H-RES group), HCD+50 mg/kg RES group (M-RES group) and HCD+25mg/kg RES group (L-RES group). After 6 months feeding, the cognitive function of mice, the pyroptosis and silent information regulator 1 (SIRT1), NLRP3, Caspase-1, IL-1β, IL-18 and TNF-α expressions in hippocampus were detected. Results were compared by the One-Way ANOVA or repeated measure ANOVA. Results Compared with HCD group, the final body mass were significantly decreased (t=-14.453, P=0.021), the level of pyroptosis in hippocampus were significantly decreased (t=-17.328, P=0.011), the learning and memory ability were significantly improved and the protein expression of SIRT1 in hippocampus was significantly increased (t=32.812, P＜0.001), while the protein expressions of NLRP3、Caspase-1、IL-1β、IL-18 and TNF-α were significantly decreased (t=-28.462, P=0.003; t=-38.148, P＜0.001; t=-38.809, P＜0.001; t=-47.239, P＜0.001; t=-48.811, P＜0.001) in H-RES group. The final body mass, the level of pyroptosis in hippocampus, the learning and memory ability and the protein expression of SIRT1, NLRP3, Caspase-1, IL-1β, IL-18 and TNF-α were not statistically different (t=12.012, P=0.132; t=-14.252, P=0.104; t=-19.219, P=0.083; t=-7.252, P=0.512; t=-15.252, P=0.286; t=-21.252, P=0.068) in L-RES group. Conclusion RES has concentration effect, and it can prevent diet- induced obesity in the mice and ameliorate cognitive function of the mice through increasing the expression of SIRT1 and inhibiting the activation of NLRP3 inflammasome-pyroptosis signal pathway in hippocampus. |
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| Keywords: | Resveratrol SIRT1 NLRP3 inflammasome Pyroptosis Obesity |
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