ensiyeh joneidi

Aluminum is a component of environmental pollutants, which causes neurotoxicity. Berberine is in the group of plant-derived alkaloids such as barberry and its beneficial therapeutic properties in various diseases have been proven. The aim of the present study was to investigate the protective effect of berberine on aluminum-induced neurotoxicity.

In this experimental study, 32 male Wistar rats were randomly divided into 4 groups: sham, berberine-receiving sham, lesions-seeing and berberine-receiving lesions. To induce neurotoxicity, a solution of aluminum chloride (AlCl3) dissolved in distilled water was injected at 5 µL at a dose of 0.37 mg/kg to the left of the dorsal hippocampus. The treated rats received 100 mg/kg of berberine daily from one hour before surgery to one week after surgery and orally. In the fourth week, all groups were tested for behavioral learning and memory using the shuttle box. At the end, malondialdehyde, protein, ROS levels and acetylcholinesterase activity were measured. The results were analyzed using one-way ANOVA test and Tukey test.

In the treated AlCl3 group compared to the AlCl3 group, the initial delay was not significantly different but the delay during transit was significantly increased. MDA and ROS levels and acetylcholinesterase activity showed a significant decrease.

The results of this study showed that although treatment with berberine in the lesion group by aluminum chloride did not cause a significant difference in learning in rats, but it significantly improved memory, significantly reduced malondialdehyde, significantly reduced oxygen free radical levels and significantly reduced activity. Acetylcholinesterase and it can be said that berberine with antioxidant properties improved memory and neuroprotection against neurotoxicity caused by aluminum chloride.

The liver is the largest gland in the body with multiple functions. Methotrexate causes acute and chronic liver damage. In this study, the effects of diosgenin were investigated as a steroidal sapogenin on mitochondrial membrane potential (MMP) and neutrophil infiltration activity in a methotrexate-induced liver injury model in male rats.

40 rats in 5 groups; control, control treated with diosgenin 50 mg/kg, methotrexate at a dose of 20 mg/kg (i.p) and two groups treated with diosgenin at doses 10, 50 mg/kg (gavage) were divided. The rats were anesthetized and the liver tissue was isolated after killing. After tissue homogeneity, neutrophil infiltration activity and mitochondrial membrane potential were measured. For statistical analysis, one-way ANOVA and Tukey post-test were used, and the significance level was p <0.05.

The potential of the mitochondrial membrane in the methotrexate group treated with diosgenin 10 mg/kg was significantly reduced compared to the control group and in the group treated with diosgenin 50 mg/kg was significantly increased compared to methotrexate. On the other hand, myeloperoxidase increased significantly in the methotrexate group and treated with diosgenin 10 mg/kg compared to the control group and decreased significantly in the group treated with diosgenin 50 mg/kg compared to the methotrexate group.

Diosgenin at a dose of 50 mg/kg in the methotrexate-induced liver injury model was able to improve mitochondrial health and reduced neutrophil infiltration.

Methotrexate can induce testicular tissue damage and infertility by increasing the activity myeloperoxidase and destroying mitochondrial membrane. Diosgenin is a steroidal sapogenin with antioxidant properties. The aim of this study was to evaluate the effects of diosgenin on mitochondrial membrane potential (MMP) and neutrophil infiltration in methotrexate-induced testicular injury in the rat.

40 rats were divided into 5 groups: control, diosgenin-treated control with a dose of 50 mg/kg, methotrexate, two groups of diosgenin-treated methotrexate at doses of 10 or 50 mg/kg. Methotrexate at a dose of 20 mg/kg was injected intraperitoneally one day after diosgenin administration. Diosgenin was administered daily for two weeks at doses of 10 or 50 mg/kg. At the end, the rats were anesthetized and the testis was removed. MPO and MMP in testicular tissue were measured. For statistical analysis, one-way ANOVA and Tukey post-test were used.

The MMP of the methotrexate group showed a significant decrease compared to the control group (p=0.003). The diosgenin-treated methotrexate group at a dose of 50 mg/kg showed a significant increase as compared to the methotrexate group (p=0.008). The level of MPO in the methotrexate group showed a significant increase as compared to the control group (p=0.009). The diosgenin-treated methotrexate group at a dose of 50 mg/kg showed a significant decrease as compared to the methotrexate group (p=0.039).

Diosgenin reduces the harmful effects of methotrexate on MPO and MMP in testicular tissue.