Liu Huihui, Feng Jun, Liu Jianhe, Cheng Choufu, H U Guoheng
{"title":"江孜消斑片对高脂饮食诱导的动脉粥样硬化小鼠的toll样受体4/核因子-kappa B/nod样受体蛋白3信号通路的疗效。","authors":"Liu Huihui, Feng Jun, Liu Jianhe, Cheng Choufu, H U Guoheng","doi":"10.19852/j.cnki.jtcm.20231121.002","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To study the effect of Jiangzhi Xiaoban tablet (, JZXB) on toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/Nod-like receptor protein 3 (NLRP3) signaling pathway expression in atherosclerosis (AS) mice by establishing a mouse model of AS, and to explore its mechanism of prevention and treatment of AS.</p><p><strong>Methods: </strong>Sixty-four male C57BL/6J mice were randomly divided into two groups, 12 in the normal control group and 52 in the model group (MOD). Seven weeks later, two mice in each of the above two groups were randomly sacrificed, and the whole aortic tissue of the mice was taken out for hematoxylin-eosin staining. After successful modeling, 50 mice in the modeling group were randomly divided into 5 groups: MOD, atorvastatin group (ATO), low-dose group of JZXB (JZXB-L), middle-dose group of JZXB (JZXB-M), and high-dose group of JZXB (JZXB-H), 10 mice in each group. The mice in each group were killed after 6 weeks of preventive administration. HE staining was used to observe the pathological changes of aorta in AS mice. The levels of serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were detected by automatic biochemical analyzer. The levels of inflammatory factor interleukin-1β (IL-1β) were detected by enzyme linked immunosorbent assay. The expression of TLR4, NF-κB and NLRP3 proteins in aortic tissue was detected by immunohistochemistry.</p><p><strong>Results: </strong>Compared with the MOD, the levels of serum TC, TG and LDL-C in the JZXB-H and ATO were significantly decreased, while the level of HDL-C was significantly increased. The levels of serum TG, LDL-C in the JZXB-M were significantly decreased, and the level of HDL-C was significantly increased. Compared with the MOD, the levels of IL-1β were significantly decreased, aortic lesions were significantly improved, and the expression of TLR4, NF-κB, and NLRP3 proteins in the aortic tissue was significantly decreased in the JZXB-H, JZXB-M, and ATO.</p><p><strong>Conclusion: </strong>JZXB has inhibitory effect on atherosclerosis in mice, and its mechanism may be through regulating the TLR4/NF-κB/NLRP3 signaling pathway and reducing the inflammatory response, so as to play a role in inhibiting atherosclerosis.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 1","pages":"88-94"},"PeriodicalIF":0.0000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774719/pdf/","citationCount":"0","resultStr":"{\"title\":\"Efficacy of Jiangzhi Xiaoban tablet on toll-like receptor 4/nuclear factor-kappa B/nod-like receptor protein 3 signaling pathway in mice with atherosclerosis induced by high-fat diet.\",\"authors\":\"Liu Huihui, Feng Jun, Liu Jianhe, Cheng Choufu, H U Guoheng\",\"doi\":\"10.19852/j.cnki.jtcm.20231121.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To study the effect of Jiangzhi Xiaoban tablet (, JZXB) on toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/Nod-like receptor protein 3 (NLRP3) signaling pathway expression in atherosclerosis (AS) mice by establishing a mouse model of AS, and to explore its mechanism of prevention and treatment of AS.</p><p><strong>Methods: </strong>Sixty-four male C57BL/6J mice were randomly divided into two groups, 12 in the normal control group and 52 in the model group (MOD). Seven weeks later, two mice in each of the above two groups were randomly sacrificed, and the whole aortic tissue of the mice was taken out for hematoxylin-eosin staining. After successful modeling, 50 mice in the modeling group were randomly divided into 5 groups: MOD, atorvastatin group (ATO), low-dose group of JZXB (JZXB-L), middle-dose group of JZXB (JZXB-M), and high-dose group of JZXB (JZXB-H), 10 mice in each group. The mice in each group were killed after 6 weeks of preventive administration. HE staining was used to observe the pathological changes of aorta in AS mice. The levels of serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were detected by automatic biochemical analyzer. The levels of inflammatory factor interleukin-1β (IL-1β) were detected by enzyme linked immunosorbent assay. The expression of TLR4, NF-κB and NLRP3 proteins in aortic tissue was detected by immunohistochemistry.</p><p><strong>Results: </strong>Compared with the MOD, the levels of serum TC, TG and LDL-C in the JZXB-H and ATO were significantly decreased, while the level of HDL-C was significantly increased. The levels of serum TG, LDL-C in the JZXB-M were significantly decreased, and the level of HDL-C was significantly increased. Compared with the MOD, the levels of IL-1β were significantly decreased, aortic lesions were significantly improved, and the expression of TLR4, NF-κB, and NLRP3 proteins in the aortic tissue was significantly decreased in the JZXB-H, JZXB-M, and ATO.</p><p><strong>Conclusion: </strong>JZXB has inhibitory effect on atherosclerosis in mice, and its mechanism may be through regulating the TLR4/NF-κB/NLRP3 signaling pathway and reducing the inflammatory response, so as to play a role in inhibiting atherosclerosis.</p>\",\"PeriodicalId\":94119,\"journal\":{\"name\":\"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan\",\"volume\":\"44 1\",\"pages\":\"88-94\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10774719/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.19852/j.cnki.jtcm.20231121.002\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.19852/j.cnki.jtcm.20231121.002","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
研究目的通过建立动脉粥样硬化(AS)小鼠模型,研究江浙夏枯草片(JZXB)对动脉粥样硬化(AS)小鼠体内toll样受体4(TLR4)/核因子-kappa B(NF-κB)/Nod样受体蛋白3(NLRP3)信号通路表达的影响,并探讨其防治AS的机制:将64只雄性C57BL/6J小鼠随机分为两组,正常对照组12只,模型组(MOD)52只。七周后,随机处死上述两组各两只小鼠,取出小鼠的整个主动脉组织进行苏木精-伊红染色。建模成功后,将建模组的 50 只小鼠随机分为 5 组:MOD组、阿托伐他汀组(ATO)、JZXB低剂量组(JZXB-L)、JZXB中剂量组(JZXB-M)、JZXB高剂量组(JZXB-H),每组10只。各组小鼠在预防性给药 6 周后处死。HE 染色观察 AS 小鼠主动脉的病理变化。用自动生化分析仪检测血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)的水平。酶联免疫吸附试验检测了炎症因子白细胞介素-1β(IL-1β)的水平。免疫组化法检测了主动脉组织中 TLR4、NF-κB 和 NLRP3 蛋白的表达:结果:与 MOD 相比,JZXB-H 和 ATO 的血清 TC、TG 和 LDL-C 水平显著降低,而 HDL-C 水平显著升高。JZXB-M的血清TG、LDL-C水平明显下降,HDL-C水平明显上升。与MOD相比,JZXB-H、JZXB-M和ATO的IL-1β水平明显降低,主动脉病变明显改善,主动脉组织中TLR4、NF-κB和NLRP3蛋白的表达明显减少:结论:JZXB对小鼠动脉粥样硬化有抑制作用,其机制可能是通过调节TLR4/NF-κB/NLRP3信号通路,减轻炎症反应,从而起到抑制动脉粥样硬化的作用。
Efficacy of Jiangzhi Xiaoban tablet on toll-like receptor 4/nuclear factor-kappa B/nod-like receptor protein 3 signaling pathway in mice with atherosclerosis induced by high-fat diet.
Objective: To study the effect of Jiangzhi Xiaoban tablet (, JZXB) on toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/Nod-like receptor protein 3 (NLRP3) signaling pathway expression in atherosclerosis (AS) mice by establishing a mouse model of AS, and to explore its mechanism of prevention and treatment of AS.
Methods: Sixty-four male C57BL/6J mice were randomly divided into two groups, 12 in the normal control group and 52 in the model group (MOD). Seven weeks later, two mice in each of the above two groups were randomly sacrificed, and the whole aortic tissue of the mice was taken out for hematoxylin-eosin staining. After successful modeling, 50 mice in the modeling group were randomly divided into 5 groups: MOD, atorvastatin group (ATO), low-dose group of JZXB (JZXB-L), middle-dose group of JZXB (JZXB-M), and high-dose group of JZXB (JZXB-H), 10 mice in each group. The mice in each group were killed after 6 weeks of preventive administration. HE staining was used to observe the pathological changes of aorta in AS mice. The levels of serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were detected by automatic biochemical analyzer. The levels of inflammatory factor interleukin-1β (IL-1β) were detected by enzyme linked immunosorbent assay. The expression of TLR4, NF-κB and NLRP3 proteins in aortic tissue was detected by immunohistochemistry.
Results: Compared with the MOD, the levels of serum TC, TG and LDL-C in the JZXB-H and ATO were significantly decreased, while the level of HDL-C was significantly increased. The levels of serum TG, LDL-C in the JZXB-M were significantly decreased, and the level of HDL-C was significantly increased. Compared with the MOD, the levels of IL-1β were significantly decreased, aortic lesions were significantly improved, and the expression of TLR4, NF-κB, and NLRP3 proteins in the aortic tissue was significantly decreased in the JZXB-H, JZXB-M, and ATO.
Conclusion: JZXB has inhibitory effect on atherosclerosis in mice, and its mechanism may be through regulating the TLR4/NF-κB/NLRP3 signaling pathway and reducing the inflammatory response, so as to play a role in inhibiting atherosclerosis.