PDF(Pubmed)
Abstract：
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.
UNASSIGNED: Thirty adult male Wistar rats were randomly divided into six groups (n=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 t-test.
UNASSIGNED: 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 (P<0.05).
UNASSIGNED: 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.
UNASSIGNED: Thirty adult male Wistar rats were randomly divided into six groups (n=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 t-test.
UNASSIGNED: 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 (P<0.05).
UNASSIGNED: 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.
摘要：
在糖尿病肾病患者中检测到许多氧化应激，导致胰岛素抵抗，损害胰腺和肾脏。肾足细胞对胰岛素不敏感会导致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实验，以检查DLBS3233对胰岛素抵抗的修复作用。
■将30只成年雄性Wistar大鼠随机分为六组（每组5只）：非糖尿病大鼠组作为阴性对照（组1）；未经治疗的糖尿病大鼠（组2）；用DLBS32334.5mg/kgBB治疗的糖尿病大鼠（组3）；9mg/kgBB（组4）；18mg/kgBB（组5）；和吡唑酮治疗的糖尿病大鼠组（作者检查了胰岛素抵抗的稳态模型评估，以证实糖尿病大鼠在DLBS3233施用之前的胰岛素抵抗。进行免疫组织化学检查肾脏抗丙二醛（MDA）抗体的表达，nephrin,波多辛,和胰岛素受体丝氨酸。数据采用方差分析和t检验进行分析。
■在DBLS3233组中，免疫组化显示肾nephrin和podocin的表达增强，以及抗MDA抗体的表达减少，随着胰岛素受体丝氨酸的减少。从统计分析来看,抗MDA抗体和胰岛素受体丝氨酸表达较低，与未治疗组相比，nephrin和podocin的表达增强（P<0.05）。
■DLBS3233通过降低MDA来降低氧化应激，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。
■将30只成年雄性Wistar大鼠随机分为六组（每组5只）：非糖尿病大鼠组作为阴性对照（组1）；未经治疗的糖尿病大鼠（组2）；用DLBS32334.5mg/kgBB治疗的糖尿病大鼠（组3）；9mg/kgBB（组4）；18mg/kgBB（组5）；和吡唑酮治疗的糖尿病大鼠组（作者检查了胰岛素抵抗的稳态模型评估，以证实糖尿病大鼠在DLBS3233施用之前的胰岛素抵抗。进行免疫组织化学检查肾脏抗丙二醛（MDA）抗体的表达，nephrin,波多辛,和胰岛素受体丝氨酸。数据采用方差分析和t检验进行分析。
■在DBLS3233组中，免疫组化显示肾nephrin和podocin的表达增强，以及抗MDA抗体的表达减少，随着胰岛素受体丝氨酸的减少。从统计分析来看,抗MDA抗体和胰岛素受体丝氨酸表达较低，与未治疗组相比，nephrin和podocin的表达增强（P<0.05）。
■DLBS3233通过降低MDA来降低氧化应激，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。
