Widya Wasityastuti
Department of Physiology, Medical Faculty, Gadjah Mada University, Yogyakarta, Indonesia

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Antifibrotics and Antioxidants of Chlorogenic Acid (CGA) Inhibits Toll- Like Receptors (TLR-4) as a Marker of Liver Fibrotic Rosdiana Naibey; Widya Wasityastuti; Nungki Anggorowati; Nur Arfian
Green Medical Journal Vol 3 No 2 (2021): Green Medical Journal
Publisher : Fakultas Kedokteran Universitas Muslim Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33096/gmj.v3i2.87

Abstract

Introduction: Chlorogenic Acid (CGA) is an antifibrotic and antioxidant for fibrotic tissues. These double roles be able to inhibit or fibrotic tissues chains because of internal and external issues. For example, virus, bacteria or other pathogens and also by drugs, alcohol, cigarettes, etc. as external factor that affect quality of body tissues. Toll-Like Receptor-4 (TLR-4) as a marker fibrotic tissues. It is a key for researcher could be find out by expression performance. The aim of this study is to reveal the CGA as a candidate of antifibrotic & antioxidant in liver fibrosis induced by CCL4. Methods: This is pure experimental research with a simple experimental design or post-test only control group design. A total 29 mices of 2.5-month-old male Swiss mice with weigh 35-40 grams divided into 6 groups: 3 groups of controls (injected by natrium chloride, CGA, and CCL4) and 3 groups of treated (injected by CGA doses 42 mg/kg, 63 mg/kg or 84 mg/kg). The liver organ was used to examine the expression of TLR-4 by rtPCR. This research revealed that expression of TLR-4 lower than the CCL4 control group (respectively, p=0.042; p=0.005; p=0.006; and p=0.001). The higher dose of CGA showed greater ability as an anti-fibrotic through inhibiting the expression of TLR-4. Some research found the expression of TLR-4 has been decreased by treatment of Chlorogenic Acid (CGA). Conclusion: To sum up, CGA has double roles to repair liver fibrotic tissues. The greater doses of CGA, the stronger inhibition of TLR-4 expression.