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Published on: November 18, 2022
Fasudil mesylate protects PC12 cells from oxidative stress injury via the Bax-mediated pathway
Qin Li1, Dong Liu, Xianju Huang
1Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
We previously reported that fasudil mesylate (FM) improves neurological deficit and neuronal damage in rats with ischemia following middle cerebral artery occlusion and reperfusion in vivo. In this study, the properties of FM on hydrogen peroxide (H(2)O(2))-induced oxidative stress insult in cultured PC12 cells as well as the underlying mechanisms were investigated in vitro. Pretreatment with FM (5, 10 μM) prior to H(2)O(2) exposure significantly elevated cell viability, reduced cell apoptosis by MTT assay, LDH assay, Hoechst 33258 dye staining, and FM also decreased the accumulation of reactive oxygen species (ROS) by DCFH-DA staining and NBT test. Furthermore, FM also reversed the upregulation of Bax/Bcl-2 ratio, the downstream cascade following ROS. FM protected PC12 cells from oxidative stress insult via downregulating the Bax/Bcl-2 ratio. These findings indicate that a direct effect of fasudil mesylate on PC12 cells may be partly responsible for its protective effect against oxidative stress injury.
Insights
Fasudil mesylate (FM) protects cultured PC12 cells against oxidative stress by reducing reactive oxygen species (ROS) and apoptosis. This neuroprotective effect involves downregulating the Bax/Bcl-2 ratio, indicating a direct cellular mechanism.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Ischemic stroke causes neuronal damage due to oxidative stress.
- Fasudil mesylate (FM) has shown promise in improving outcomes after ischemic stroke in vivo.
- The direct cellular mechanisms of FM's protective effects against oxidative stress require further elucidation.
Purpose of the Study:
- To investigate the protective properties of fasudil mesylate (FM) against hydrogen peroxide (H(2)O(2))-induced oxidative stress in cultured PC12 cells.
- To elucidate the underlying molecular mechanisms of FM's neuroprotective effects in vitro.
- To determine if FM has a direct effect on PC12 cells against oxidative injury.
Main Methods:
- PC12 cells were pretreated with FM (5, 10 μM) before exposure to H(2)O(2).
- Cell viability and apoptosis were assessed using MTT assay, LDH assay, and Hoechst 33258 dye staining.
- Reactive oxygen species (ROS) accumulation was measured by DCFH-DA staining and NBT test.
- Changes in the Bax/Bcl-2 ratio were analyzed to understand downstream effects.
Main Results:
- FM pretreatment significantly increased cell viability and reduced apoptosis in H(2)O(2)-exposed PC12 cells.
- FM decreased the accumulation of reactive oxygen species (ROS) in a dose-dependent manner.
- FM reversed the H(2)O(2)-induced upregulation of the Bax/Bcl-2 ratio, indicating modulation of apoptotic pathways.
- These results suggest FM exerts a direct protective effect on PC12 cells against oxidative stress.
Conclusions:
- Fasudil mesylate (FM) demonstrates significant neuroprotective effects against oxidative stress in cultured PC12 cells.
- FM mitigates oxidative damage by reducing reactive oxygen species (ROS) and inhibiting apoptosis.
- The mechanism involves downregulating the Bax/Bcl-2 ratio, highlighting a direct cellular action of FM.
