Berberine protects myocardial cells against anoxia‑reoxygenation injury via p38 MAPK‑mediated NF‑κB signaling pathways

Abstract

Ischemic heart disease is a leading cause of mortality and occurs due to coronary arterial atherosclerosis, vascular cavity stenosis and occlusion. It has previously been demonstrated that berberine treatment may ameliorate and help to prevent cardiovascular diseases due to its anti-inflammatory and anti-apoptotic effects in myocardial cells. However, the potential signaling mechanisms mediated by berberine in the progression of myocardial injury remain to be elucidated. The aim of the present study was to investigate the therapeutic effects of berberine and its potential mechanism in a mouse model of myocardial cell injury. The results revealed that berberine treatment downregulated the serum expression of inflammatory factors, including interleukin (IL)-6, tumor necrosis factor-α, IL-10 and IL-17A in mice with anoxia-reoxygenation injury. Berberine treatment also decreased myocardial cell apoptosis following anoxia-reoxygenation injury via regulating the expression of apoptosis-associated genes. Histological analysis revealed that the area, circumference fragmentation and segmentation of myocardial cells were significantly decreased by berberine treatment compared with the control group. The body weight, blood lipid levels, blood pressure and heart rate were markedly improved in mice with anoxia-reoxygenation injury following berberine treatment compared with untreated mice. The expression of p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB expression was downregulated in myocardial cells from in mice with anoxia-reoxygenation injury following berberine treatment compared with untreated mice. However, p38 MAPK overexpression ameliorated the berberine-induced decrease in NF-κB activity and expression, as well as the berberine-induced inhibition of myocardial apoptosis in myocardial cells isolated from experimental mice. In conclusion, the results of the present study indicate that berberine is able to decrease the expression of inflammatory cytokines expression and inhibit myocardial cell apoptosis via downregulating the p38 MAPK-mediated NF-κB signaling pathway. These results suggest that berberine may be an effective treatment for anoxia-reoxygenation injury.

Complementary Chinese Herbal Medicine Therapy Improves Survival in Patients With Pemphigus: A Retrospective Study From a Taiwan-Based Registry

“…Natural compounds including coptisine, berberine, and palmatine have been detected in Huang–Lian ( Rhizoma Coptidis ; Coptis chinensis Franch. ) ( Tian et al, 2017 ), with coptisine and berberine exhibiting anti-inflammatory activity through inhibition of both the p38 MAPK and NF-kB pathways ( Chen et al, 2017 ; Zhao et al, 2019 ). Natural compounds including kaempferol, ursolic acid, and rutin have been detected in Jin–Yin–Hua ( Flos Lonicerae ; Lonicera japonica Thunb. )…”

Berberine Improves High-Fat Diet Induced Atherosclerosis and Hepatic Steatosis in Apoe-/-Mice by Down-Regulating PCSK9 via ERK1/2 Pathway

“…In vitro studies showed that both PCSK9 and HNF1a proteinlevels were decreased in BBR-treated HepG2 cells [26]. In this ApoE -/mice fed with HFD, our data indicated that BBRcould signi cantly decrease PCSK9 expression both in ApoE -/mice fed with HFD and HepG2 cells, the underlying mechanisms might through the activation of the MAPK/ERK1/2 signaling pathway, which might provide additional information regarding the potential role of BBR in anti-AS process besides of its anti-in ammatory action [27,28], reducing oxidative stress [6,29,30], and enhancingcholesterol e ux [31][32][33], which was summarized in Fig. 7.…”

Berberine attenuates atherosclerotic lesions and hepatic steatosis in ApoE-/- mice by down-regulating PCSK9 via ERK1/2 pathway

“…All these proteins were related to the process of reverse cholesterol transport. Thereby, our findings might provide additional information regarding the potential role of BBR in anti-atherosclerosis process besides of its anti-inflammatory action (28,29) reducing oxidative stress (6,30,31), and enhancing cholesterol efflux (32)(33)(34), which was summarized in Figure 7.…”