ABSTRACT
@#Introduction: Chronic kidney disease (CKD) leads to tubular injury, kidney fibrosis and anemia. These conditions are influenced by fibrotic and anti-fibrotic substances, such as Transforming Growth Factor beta-1 (TGF-β1), Hepatic Growth Factor (HGF), and Bone Morphogenic Protein-7 (BMP-7). Yacon is an herbal medicine which has not been elucidated in CKD. This study aimed to investigate the effect of ethanolic extract of Yacon leaves on attenuating renal injury in CKD model in mice. Methods: We performed 5/6 subtotal nephrectomy (SN) in male Swiss-Webster mice (3 months old, 30–40 grams) to induce chronic kidney disease, then the mice were sacrificed at day 14. The mice (n=25) were divided into five groups: one SN group, three groups of SN with administration of Yacon extract, and one group of sham operation (SO, with supplementation of 0.1% aquadest). There were three different doses of ethanolic extract of Yacon leaves: 98 mg/kg BW (SN+YK1), 49 mg/kg BW (SN+YK2), and 24.5 BW mg/kg (SN+YK3). Tubular injury, perivascular and interstitial fibrosis were quantified based on histopathological examination. Reverse-transcriptase PCR (RT-PCR) was performed to quantify HGF and BMP-7. Results: SN group demonstrated CKD with elevation of creatinine level, anemia, tubular injury, glomerulosclerosis, and fibrosis. Yacon extract treatment showed attenuation of injury with lower creatinine level, tubular injury, glomerulosclerosis and fibrosis compared to the SN group. HGF and BMP-7 mRNA expressions were higher in Yacon-treated groups than the SN group. Conclusion: Yacon treatment might ameliorate CKD through reducing fibrosis and increasing expression of anti-fibrotic genes.
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.