RESUMO
Objective: To explore the inhibitory effect of gallotannin (GLTN) on the proliferation of rat glomerular mesangial cells (GMC)induced by high sugar stimulation and the influence in the cell cycle of the rats, and to clarify the prevention effect of GLTN in the occurrence and development of diabetic nephropathy (DN). Methods:The experimental cells were divided into normal control group (D-glucose 5.5 mmol·L-1 ,NC group), high glucose group (D-glucose 30 mmol· L-1 ,HC group),high glucose + 5 mmol· L-1 3 - AB group (AB group),high glucose + 20 μmol·L-1 GLTN group (G20 group),high glucose + 40 μmol· L-1 GLTN group (G40 group).The proliferation of GMC in different groups at different time points (4,8,24,48 and 72 h)was observed by MTT assay.The changes of cell cycle of GCM under different culture conditions were examined by flow cytometry,and the expression levels of TGF-β1 and CTGF were detected by Western blotting method. Results:Compared with NC group,the proliferation levels of GMC in HC group were increased (P <0.01),and reached the peak at 48 h ;the percentage of S phase cells was increased (P <0.01).Compared with HC group,the proliferation levels of GMC in 3-AB group and GLTN group were significantly decreased (P < 0.01 ),and the percentages of S phase cells were decreased (P <0.01).Compared with NC group,the protein expression levels of TGF-β1 and CTGF in each drug group were increased (P < 0.05 or P < 0.01),but they were significantly lower than those in HC group (P < 0.01).Conclusion:GLTN can inhibit the proliferation of GMC under high sugar stimulation through arresting the cell cycle and down-regulating the expressions of TGF-β1 and CTGF and delay the occurrence and development of DN.
RESUMO
To evaluate the hepatotoxicity and nephrotoxicity of Galla Rhois (GR) toward the liver and kidney of ICR mice, alterations in related markers including body weight, organ weight, urine composition, liver pathology and kidney pathology were analyzed after oral administration of 250, 500 and 1,000 mg/kg body weight/day of gallotannin-enriched extract of GR (GEGR) for 14 days. GEGR contained 68.7+/-2.5% of gallotannin, 25.3+/-0.9% of gallic acid and 4.4+/-0.1% of methyl gallate. Also, the level of malondialdehyde (MDA), a marker of lipid peroxidation, was decreased with 19% in the serum of high dose GEGR (HGEGR)-treated mice. The body and organ weight, clinical phenotypes, urine parameters and mice mortality did not differ among GEGR-treated groups and the vehicle-treated group. Furthermore, no significant increase was observed in alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), blood urea nitrogen (BUN) and the serum creatinine (Cr) in the GEGR-treated group relative to the vehicle-treated group. Moreover, the specific pathological features induced by most toxic compounds such as CCl4 were not observed upon liver and kidney histological analysis. Overall, the results of the present study suggest that GEGR does not induce any specific toxicity in liver and kidney organs of ICR at doses of 1,000 mg/kg body weight/day, indicating that this is no observed adverse effect level (NOAEL).