How Does Curcumin Involve the Myofibrosis Process of Rabbit Valve Interstitial Cells Based on Expression Α- Smooth Muscle Actin? Study in Vitro

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I G N Iswan Rahmadi Ranuh, J. Nugroho Eko Putranto, Achmad Lefi


Introduction: Rheumatic heart valve disease is a sequela after acute rheumatic fever infection caused by an inflammatory response to streptococcal bacteria which then triggers valve damage. Elements of the immune system play an important role, in facilitating myofibroblast transdifferentiation and clearing damaged tissue of apoptotic cells. Myofibrosis arising in valve components is the main cause of valve dysfunction. Valve myofibrosis showed a significantly increased content of collagen, proteoglycan, and elastin in myofibrotic valves compared to healthy valves. Objective: To prove the inhibitory ability of curcumin on the differentiation of rabbit valve interstitial cells induced by TGF-β1 into myofibroblasts based on –SMA expression compared to controls.

Method: This study is an in vitro laboratory experimental posttest-only control group design. Valve interstitial cells isolated from heart valves of New Zealand rabbit (Oryctolagus cuniculus), induced fibrosis by administration of TGF-β1 5 ng/ml. Valve interstitial cells pretreated with TGF-β1 were treated with low-dose curcumin (20 nanoM/L) and high-dose curcumin (50 nanoM/L). Inhibition of myofibroblastic differentiation was observed by the immunocytochemical method based on SMA expression. Statistical significance was analyzed by Kruskal-Wallis statistical test with a p-value <0.05 as the limit of significance.

Result: Administration of curcumin with low doses (20 nanoM/L) and high doses (50 nanoM/L), significantly decreased TGF-β1-induced myofibroblastic differentiation of valve interstitial cells, which was characterized by decreased SMA expression in all low-dose curcumin treatment groups (20). nanoM/L) (1.40 ± 6.30) and high-dose curcumin (50 nanoM/L) (1.40 ± 8.30).

Conclusion: Curcumin can inhibit the differentiation of valve interstitial cells into myofibroblasts based on SMA expression.

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