Mohani Chandra I, Rudijanto Achmad, Aulanni'am Aulanni'am, Soeharto Setyawati
Universitas Brawijaya.
Department of Internal Medicine, Division of Endocrinology and Metabolic.
Ann Med Surg (Lond). 2023 Mar 13;85(8):3894-3900. doi: 10.1097/MS9.0000000000000308. eCollection 2023 Aug.
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.
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.
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).
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.
在糖尿病肾病患者中检测到多种氧化应激，导致胰岛素抵抗，损害胰腺和肾脏。对胰岛素不敏感的肾足细胞会导致nephrin和podocin减少，胰岛素受体丝氨酸增加。作者对糖尿病大鼠进行了一项实验，以研究DLBS3233对修复胰岛素抵抗的作用。
30只成年雄性Wistar大鼠随机分为6组（每组 = 5只）：非糖尿病大鼠组作为阴性对照（第1组）；未治疗的糖尿病大鼠组（第2组）；用4.5 mg/kg BB的DLBS3233治疗的糖尿病大鼠组（第3组）；9 mg/kg BB（第4组）；18 mg/kg BB（第5组）；以及用吡格列酮治疗的糖尿病大鼠组（第6组）。作者在对糖尿病大鼠给予DLBS3233之前，检查了胰岛素抵抗的稳态模型评估以证实胰岛素抵抗。进行免疫组织化学以检测肾抗丙二醛（MDA）抗体、nephrin、podocin和胰岛素受体丝氨酸的表达。使用方差分析和t检验对数据进行分析。
在DBLS3233组中，免疫组织化学显示肾nephrin和podocin表达增强，抗MDA抗体表达减少，同时胰岛素受体丝氨酸减少。通过统计分析，与未治疗组相比，抗MDA抗体和胰岛素受体丝氨酸表达较低，而nephrin和podocin的表达增强（P<0.05）。
DLBS3233通过降低MDA减少氧化应激，并通过增加肾nephrin和podocin的表达以及降低胰岛素受体丝氨酸来改善胰岛素抵抗。
