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The inflammatory response is implied as a target to reduce myocardial ischemia injury. Berberine (BBR), a natural component used in Chinese medicine, exerts anti-inflammatory effect. In this study, we examined the effects of berberine on ischemia induced inflammation in cardiomyocytes and the underlying mechanisms.
R descending coronary artery in Sprague Dawley rats. Western blot and quantitative reverse transcriptase-polymerase chain reaction were used for detecting the protein and mRNA expression of TLRs and the associated signaling pathways. NF-kB activation was determined by immunohistochemistry and western blot. Levels of TNF-a and IL-6 were analyzed by elisa.
Our results showed that berberine significantly inhibited inflammatory cytokine production in cardiomyocytes and reduced the expressions of nuclear factor-kB (NF-kB) after cardiomyocyte ischemia. Further study revealed that the effects of berberine on cardiac inflammation induced by ischemia was through down-regulating TLR4 expression followed by inhibition of myeloid differentiation factor 88 (MyD88), c-Jun NH2-terminal kinase (JNK), and NF-kB activation. Berberine couldn’t inhibit cardiac inflammation induced by ischemia under TLR4 inhibitor treatment.
Berberine inhibited ischemia induced cardiac inflammation by reducing cytokine production and the activation of TLR4/MyD88/JNK/NF-kB signaling pathway. Our findings suggest that berberine may serve as a new therapeutic drug for the protection of cardiomyocytes during ischemia.