DLBS3233 enhances nephrin and podocin expression also reduces oxidative stress marker and insulin receptor serine diabetic rats' podocytes.

UNLABELLED

Numerous oxidative stresses are detected in patients with diabetic kidney disease, resulting in insulin resistance that damages the pancreas and kidney. Renal podocytes insensitive to insulin lead to decreased nephrin and podocin and increased insulin receptor serine. The authors did an experiment on diabetic rats to examine the effect of DLBS3233 on repairing insulin resistance.

MATERIALS AND METHODS

Thirty adult male Wistar rats were randomly divided into six groups (=5 per group): group of nondiabetic rats as a negative control (group 1); untreated diabetic rats (group 2); diabetic rats treated with DLBS3233 4.5 mg/kg BB (group 3); 9 mg/kg BB (group 4); 18 mg/kg BB (group 5); and diabetic rats treated with pioglitazone (group 6). The authors checked Homeostatic Model Assessment for Insulin Resistance to corroborate insulin resistance prior to DLBS3233 administration in diabetic rats. Immunohistochemistry was performed to examine the expression of renal antimalondialdehyde (MDA) antibodies, nephrin, podocin, and insulin receptor serine. The data were analyzed using analysis of variance and the -test.

RESULT

In the DBLS3233 group, immunohistochemistry showed enhanced expression of renal nephrin and podocin, as well as diminished expression of anti-MDA antibody, along with decreased insulin receptor serine. From statistical analysis, anti-MDA antibodies and insulin receptor serine showed lower expression, whereas the expression of nephrin and podocin were enhanced compared to untreated groups (<0.05).

CONCLUSION

DLBS3233 reduces oxidative stress by decreasing MDA and improves insulin resistance by increasing the expression of renal nephrin and podocin as well as decreasing insulin receptor serine.