Berberine Exhibits Anti‐atherosclerotic Effects in a Mouse Model by Targeting the JAK/STAT Pathway

Abstract

Atherosclerosis, a serious and commonly diagnosed pathological condition is the main cause of coronary and cerebrovascular disorder which has a high rate of morbidity and mortality globally. In the present study effect of berberine on damage to the aorta wall induced by atherosclerosis in mice model was investigated. The results demonstrated that berberine treatment significantly (P<0.05) reverses the atherosclerosis‐induced increase in the area of the lesions in the mice aortas. Berberine treatment at 0.5, 1.0 and 2.0 mg/kg doses reduced lesion area in the aorta of atherosclerosis mice to 53.5±3.69, 39.4±3.69 and 13.8±2.12 %, respectively. Atherosclerosis‐induced up‐regulation of interleukin (IL)‐1β and IL‐6 production was down‐regulated in mice aortas on treatment with berberine. Treatment with berberine downregulated the atherosclerosis‐induced increase in expression of monocyte chemoattractant protein‐1 (MCP‐1), tumor necrosis factor (TNF)‐α, angiotensin II (AngII), Alveolar type 2 progenitor cells (AT1), and AT2 in mice aorta tissues. Moreover, berberine treatment of atherosclerosis mice led to a marked reduction in the activation of signal transducer and activator of transcription 3 (STAT3), p65, and p38 proteins. In summary, berberine treatment reverses damage associated with atherosclerosis in mice aorta walls by inhibiting the inflammatory response. It targets activation of Janus kinase (JAK)/STAT pathway and downregulated RAAS expression in atherosclerotic mice. Therefore, berberine may be developed as a potential chemotherapeutic agent for atherosclerosis treatment.