Curcumin Involve the Myofibrosis Process of Rabbit Valve Interstitial Cells based on Expression Alpha- Smooth Muscle Actin: Experimental Posttest-only Control Group Design

Abstract

Introduction: Following an acute rheumatic fever infection brought on by an inflammatory reaction to streptococcal bacteria, rheumatic heart valve disease results in valve degeneration. Elements of the immune system play an important role, in facilitating myofibroblast transdifferentiation and clearing damaged tissue of apoptotic cells. Myelofibrosis arising in valve components is the main cause of valve dysfunction. Valve myelofibrosis showed a significantly increased collagen, proteoglycan, and elastin content in myofibrotic valves compared to healthy valves. Objective: To establish curcumin’s capacity to prevent rabbit valve interstitial cells (VIC) from differentiating into myofibroblasts after being stimulated by TGF-1 by comparing the results to controls. Method: This study uses a posttest-only control group design for an in-vitro laboratory experiment. Heart VIC of a New Zealand rabbit were isolated (Oryctolagus cuniculus), and induced fibrosis by administration of TGF-β1 5 ng/mL. VIC pretreated with TGF-β1 were treated with low-dose curcumin (20 nanoM/L) and high-dose curcumin (50 nanoM/L). The immunocytochemical method based on SMA expression observed the inhibition of myofibroblastic differentiation. 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 VIC, 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 potentially prevent the development of SMA-expressing VIC into myofibroblasts.

Oral Combination of Vitamin B1, B6, and B12 Supplementation on CD4+ T Cell and IFN-γ in Pulmonary Tuberculosis Patients with First-Line Opioid agonist therapy

“…PPAR-γ is expressed in large quantities in alveolar macrophages and is essential for differentiation. The function of PPAR-γ activation against mycobacterial infection was shown to positively regulate prostaglandin (PG) E2 production in infected macrophages (23). Thus, PPAR-γ activation will increase cyclooxygenase (COX2) expression and PGE2 production in macrophages infected with M. tuberculosis so that macrophages will become activated macrophages and can kill M. tuberculosis more strongly (24).…”