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.

Abstract

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.