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Nimesulide prevents oxidative stress damage following transient forebrain ischemia in the rat hippocampus
Abdulhakeem A Al-Majed1, Abdulaziz A Al-Yahya, Yousifa Asiri
1College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Kingdom of Saudi Arabia. majed107@hotmail.com
Abstract:
This investigation was performed to evaluate the effects of nimesulide (NIM), a selective cyclo-oxygenase-2 (COX-2) inhibitor, on forebrain ischemia-induced in vivo oxidative stress damage in the rat hippocampus. Hippocampal tissue glutathione (GSH) and malondialdehyde (MDA) contents, the activities of the antioxidants superoxide dismutase (SOD) and catalase as well as nitric oxide (NO) concentration were estimated. A clinically relevant dose of NIM (18 mg x kg(-1) x d(-1), p.o.) was administered immediately after induction of forebrain ischemia for 7 consecutive days. Forebrain ischemia induced oxidative stress after 7 days manifested by significant decrease in GSH and increase in MDA levels as compared to control (p < 0.05). Also, in rats subjected to ischemia, SOD and catalase activities were decreased significantly compared to the control group (p < 0 .05). On the other hand, ischemic rats showed a significant increase in NO concentration compared to those in the control group (p < 0.05). Treatment with NIM protected the rats from ischemia-induced oxidative stress as evident by normalization of measured parameters. The present study indicates the ability of NIM to reduce oxidative stress induced by transient forebrain ischemia. This suggests that the induction of COX-2 might be involved in transient forebrain ischemia-induced oxidative damage and hence the selective COX-2 inhibitors might be a valuable therapeutic strategy against ischemic brain injury.
Insights
Nimesulide (NIM), a selective cyclo-oxygenase-2 inhibitor, reduced oxidative stress in rats following forebrain ischemia. This indicates NIM
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Transient forebrain ischemia causes significant oxidative stress in the rat hippocampus.
- Ischemia leads to decreased antioxidant levels (glutathione, superoxide dismutase, catalase) and increased oxidative damage markers (malondialdehyde, nitric oxide).
Purpose of the Study:
- To evaluate the neuroprotective effects of nimesulide (NIM), a selective cyclo-oxygenase-2 (COX-2) inhibitor, against ischemia-induced oxidative stress in the rat hippocampus.
- To investigate the role of COX-2 in transient forebrain ischemia-induced oxidative damage.
Main Methods:
- Induction of transient forebrain ischemia in rats.
- Administration of nimesulide (18 mg/kg/day) for 7 days post-ischemia.
- Measurement of hippocampal glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase, and nitric oxide (NO) levels.
Main Results:
- Forebrain ischemia significantly decreased GSH, SOD, and catalase activities while increasing MDA and NO levels in the hippocampus.
- Nimesulide treatment normalized these biochemical parameters, indicating a reduction in oxidative stress.
- NIM administration demonstrated significant protection against ischemia-induced oxidative damage.
Conclusions:
- Nimesulide effectively reduces oxidative stress associated with transient forebrain ischemia in rats.
- The findings suggest that COX-2 induction plays a role in ischemia-induced oxidative damage.
- Selective COX-2 inhibitors like nimesulide may offer a potential therapeutic strategy for ischemic brain injury.
