آزاده امین زاده

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive neuronal dysfunction. Growing evidence has shown that oxidative stress plays a crucial role in the pathogenesis of Parkinson's disease. Correspondingly, the current study evaluated the protective effect of topiramate in 6-hydroxydopamine induced oxidative stress and apoptosis in PC12 cells as an in vitro model for PD.

PC12 cells, a cellular model of PD, were treated with topiramate for 24 h. Then they were treated with 75 μM 6-hydroxydopamine for 24 h. Cell viability was examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-tetrazolium bromide (MTT) assay. Intracellular reactive oxygen species (ROS) levels were measured using 2, 7 dichlorodihydrofluorescein diacetate (DCF-DA) assay. The levels of lipid peroxidation and total antioxidant power (TAP) were also measured.

Remarkably, topiramate at concentration of 8 μM increased survival of PC12 cells exposed to 6-hydroxydopamine. Cell viability of PC12 cells on 6-hydroxydopamine was decreased compared to controls, which was reversed by topiramate. Topiramate also reduced intracellular reactive oxygen species (ROS) level and cellular lipid peroxidation. In addition, topiramate significantly increased total antioxidant power in 6-OHDA-treated cells.

Findings of this study showed that the topiramate protects PC12 cells against 6-OHDA-induced neurotoxicity through its potent antioxidant activity

Morphine has a high addictive potential and can be abused. Long-term use of morphine is associated with some pathological consequences including neurotoxicity, neuronal dysfunction, oxidative stress and apoptosis. Increasing evidence has shown that melatonin has antioxidant and antiapoptosis properties. However, its effects on morphine-induced neurotoxicity in PC12 cells have not been studied. This study was carried out to evaluate protective effect of melatonin against morphine-induced neurotoxicity in PC12 cells.

PC12 cells were treated for 24 h with several doses of melatonin (10, 25, 40, and 50 μM). The cells were then treated with 3.2 mM morphine for 24 h. The viability of PC12 cells was measured using MTT assay. The antioxidant activity of melatonin was evaluated by measuring the levels of reactive oxygen species (ROS), lipid peroxidation (LPO) and total thiol groups, and total antioxidant power (TAP).

Melatonin significantly enhanced the viability of PC12 cells and protected the cells against morphine-induced overproduction of ROS. Melatonin has increased TAP and total thiol groups and decreased LPO.

Melatonin attenuates neurotoxicity of morphine in PC12 cells via antioxidant activity.

Metformin is an anti-diabetic drug, which may be a novel therapeutic option for treatment of atherosclerosis. The current study evaluates protective capacity of metformin in hydrogen peroxide (H2O2)-induced oxidative stress in human umbilical vein endothelial cells (HUVECs).

Endothelial cells were treated with metformin for 24 h. Then they were treated with 0.5 mM H2O2 for 2h. Cell viability was measured by 3‑(4,5-dimethylthiazol-2-yl)-2, 5‑diphenyltetrazolium bromide (MTT) assay. Reactive oxygen species (ROS) levels were measured using 2, 7 dichlorodihydrofluorescein diacetate (DCF-DA) assay. Lipid peroxidation (LPO), total thiol groups and total antioxidant power (TAP) were also evaluated.

Metformin at concentration of 20 μM increased survival of HUVECs exposed to H2O2. ROS and MDA levels increased in H2O2-treated endothelial cells. Metformin could significantly decrease H2O2-induced ROS and MDA elevation. It also increased total thiol groups and TAP.

Metformin protects HUVECs against the oxidative stress and apoptosis induced by H2O2.

Hyperglycemia which occurs in diabetes is one of the main factors which can lead to serious complications such as diabetic neuropathy. There is evidence that allopurinol has neuroprotective effect against many types of damaging stimuli. The present study investigated the effects of allopurinol on high glucose induced neurotoxicity in PC12 cells as a suitable in-vitro model for evaluation of neuronal functions.
Material and Neurotoxicity was induced by high glucose concentration, and cells were exposed to allopurinol in the presence or absence of high glucose concentration. Cell viability was assessed by MTT assay. Biochemical markers of oxidative stress were investigated by measurement of lipid peroxidation (LPO), total thiol groups, and total antioxidant power (TAP).
The present results indicated that allopurinol significantly inhibited high glucose- induced cell death in PC12 cells. Furthermore, treatment with allopurinol decreased lipid peroxidation level. It also increased the total thiol groups and TAP.
These findings showed protective effects of allopurinol on HG-induced cell death in PC12 cells, which may be related to its antioxidant effect and inhibition of oxidative stress.