Uric Acid Induces Inflammation, Hepatocyte Apoptosis and Deterioration of Liver Function
- Author:
Dwi Cahyani Ratna Sari
1
;
Rina Nofrienis
2
;
Muhammad Mansyur Romi
1
;
Untung Tranggono
3
;
Eryna Ayu Nugra Desita
1
;
Nur Arfian
1
Author Information
- Publication Type:Journal Article
- Keywords: Hyperuricemia, Liver, TLR-4, MCP-1, Hepatocyte apoptosis
- From:Malaysian Journal of Medicine and Health Sciences 2020;16(Supp 3,June):49-55
- CountryMalaysia
- Language:English
- Abstract: Introduction: Uric acid is a common cause of liver tissue damage due to its hepatotoxic effect. This study is aimed to investigate: (1) the effect of uric acid on liver damage which can be seen from the serum levels of SGOT and SGPT, (2) the inflammatory response demonstrated by TLR-4 and MCP-1 mRNA expression, and (3) the proportion of hepatocytes apoptosis in mice. Methods: A total of 25 adult male Swiss-Webster mice were divided into five groups: one control group and four uric acid groups (AU7, AU14, AU21 and AU28). The uric acid groups were administered with 125 mg/kgBW uric acid for 7, 14, 21, and 28 days. Following the treatment, mice were terminated and the liver was harvested. Blood sample was taken from retro-orbital vein to assess serum uric acid, SGOT, and SGPT levels. RT-PCR was performed to examine the mRNA expressions of TLR-4 and MCP-1. TUNEL staining was used to assess the proportion of apoptotic hepatocytes. Results: Induction of uric acid caused hyperuricemia, increased expression of TLR-4 and MCP-1 mRNA significantly (p<0.05) which indicated an inflammatory reaction. The levels of SGOT and SGPT were elevated significantly (p<0.05), as well as the number of hepatocyte apoptosis (p<0.05). Conclusion: Hyperuricemia affected the inflammatory response by increasing the mRNA expression of TLR-4 and MCP-1. An increased number of apoptotic hepatocytes was likely caused by the ongoing inflammatory reaction during the induction of uric acid.
- Full text:11.2020my07181.pdf
