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Pharmacological evidence for connection of nitric oxide-mediated pathways in neuroprotective mechanism of ischemic postconditioning in mice.

Gulati P, Singh N - J Pharm Bioallied Sci (2014)

Bottom Line: Various triggers, mediators and end effectors are suggested to contribute to the protective effect of PoCo.Further a rise in acetylcholinesterase activity and TBARS level along with fall in brain nitrite/nitrate and glutathione levels was also noted. iPoCo consisting of three episodes of 10 s carotid artery occlusion and reperfusion (instituted immediately after BCAO) significantly attenuated infarct size, memory impairment, motor incoordination as well as altered biochemicals. iPoCo-induced neuroprotective effects were significantly abolished by pretreatment of L-NAME, a nonselective NOS inhibitor.It may be concluded that the nitric oxide pathway probably plays a vital role in the neuroprotective mechanism of iPoCo.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India.

ABSTRACT

Introduction: Postconditioning (PoCo) is an adaptive phenomenon whereby brief repetitive cycles of ischemia with intermittent reperfusion instituted immediately after prolonged ischemia at the onset of prolonged reperfusion elicit tissue protection. PoCo is noted to exert a protective effect in various organs like heart, liver, kidney and brain. Various triggers, mediators and end effectors are suggested to contribute to the protective effect of PoCo. However, the neuroprotective mechanism of PoCo is poorly understood.

Objectives: The present study has been designed to investigate the role of nitric oxide pathway in the neuroprotective mechanism of ischemic postconditioning (iPoCo) employing a mouse model of global cerebral ischemia and reperfusion-induced injury.

Materials and methods: Bilateral carotid artery occlusion (BCAO) of 12 min followed by reperfusion for 24 h was employed to produce ischemia and reperfusion (I/R)-induced cerebral injury in mice. Cerebral injury was assessed in the terms of cerebral infarct, memory impairment and motor in-coordination. Brain nitrite/nitrate; acetylcholinesterase activity, thiobarbituric acid reactive species (TBARS) and glutathione level were also estimated.

Results: BCAO followed by reperfusion produced a significant rise in cerebral infarct size, memory impairment and motor incoordination. Further a rise in acetylcholinesterase activity and TBARS level along with fall in brain nitrite/nitrate and glutathione levels was also noted. iPoCo consisting of three episodes of 10 s carotid artery occlusion and reperfusion (instituted immediately after BCAO) significantly attenuated infarct size, memory impairment, motor incoordination as well as altered biochemicals. iPoCo-induced neuroprotective effects were significantly abolished by pretreatment of L-NAME, a nonselective NOS inhibitor.

Conclusion: It may be concluded that the nitric oxide pathway probably plays a vital role in the neuroprotective mechanism of iPoCo.

No MeSH data available.


Related in: MedlinePlus

Effect of various interventions on motor performance (% resistance to lateral push) using the lateral push test. Each group represents mean ± S.E.M. a=P<0.05 vs sham, b=P<0.05 vs control, c=P<0.05 vs PoCo. PoCo: Postconditioning
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Figure 4: Effect of various interventions on motor performance (% resistance to lateral push) using the lateral push test. Each group represents mean ± S.E.M. a=P<0.05 vs sham, b=P<0.05 vs control, c=P<0.05 vs PoCo. PoCo: Postconditioning

Mentions: Global cerebral ischemia followed by reperfusion produced a significant decrease in percentage resistance to lateral push noted after 24 h of reperfusion in the control group, when compared to the sham group. iPoCo significantly prevented I/R-induced decrease in percentage resistance to lateral push. Further, pretreatment of L-NAME significantly (P < 0.05) abolished iPoCo-induced effect on resistance to lateral push. However, L-NAME did not modify decrease in percentage resistance to lateral push of ischemic control animals [Figure 4].


Pharmacological evidence for connection of nitric oxide-mediated pathways in neuroprotective mechanism of ischemic postconditioning in mice.

Gulati P, Singh N - J Pharm Bioallied Sci (2014)

Effect of various interventions on motor performance (% resistance to lateral push) using the lateral push test. Each group represents mean ± S.E.M. a=P<0.05 vs sham, b=P<0.05 vs control, c=P<0.05 vs PoCo. PoCo: Postconditioning
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4231382&req=5

Figure 4: Effect of various interventions on motor performance (% resistance to lateral push) using the lateral push test. Each group represents mean ± S.E.M. a=P<0.05 vs sham, b=P<0.05 vs control, c=P<0.05 vs PoCo. PoCo: Postconditioning
Mentions: Global cerebral ischemia followed by reperfusion produced a significant decrease in percentage resistance to lateral push noted after 24 h of reperfusion in the control group, when compared to the sham group. iPoCo significantly prevented I/R-induced decrease in percentage resistance to lateral push. Further, pretreatment of L-NAME significantly (P < 0.05) abolished iPoCo-induced effect on resistance to lateral push. However, L-NAME did not modify decrease in percentage resistance to lateral push of ischemic control animals [Figure 4].

Bottom Line: Various triggers, mediators and end effectors are suggested to contribute to the protective effect of PoCo.Further a rise in acetylcholinesterase activity and TBARS level along with fall in brain nitrite/nitrate and glutathione levels was also noted. iPoCo consisting of three episodes of 10 s carotid artery occlusion and reperfusion (instituted immediately after BCAO) significantly attenuated infarct size, memory impairment, motor incoordination as well as altered biochemicals. iPoCo-induced neuroprotective effects were significantly abolished by pretreatment of L-NAME, a nonselective NOS inhibitor.It may be concluded that the nitric oxide pathway probably plays a vital role in the neuroprotective mechanism of iPoCo.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India.

ABSTRACT

Introduction: Postconditioning (PoCo) is an adaptive phenomenon whereby brief repetitive cycles of ischemia with intermittent reperfusion instituted immediately after prolonged ischemia at the onset of prolonged reperfusion elicit tissue protection. PoCo is noted to exert a protective effect in various organs like heart, liver, kidney and brain. Various triggers, mediators and end effectors are suggested to contribute to the protective effect of PoCo. However, the neuroprotective mechanism of PoCo is poorly understood.

Objectives: The present study has been designed to investigate the role of nitric oxide pathway in the neuroprotective mechanism of ischemic postconditioning (iPoCo) employing a mouse model of global cerebral ischemia and reperfusion-induced injury.

Materials and methods: Bilateral carotid artery occlusion (BCAO) of 12 min followed by reperfusion for 24 h was employed to produce ischemia and reperfusion (I/R)-induced cerebral injury in mice. Cerebral injury was assessed in the terms of cerebral infarct, memory impairment and motor in-coordination. Brain nitrite/nitrate; acetylcholinesterase activity, thiobarbituric acid reactive species (TBARS) and glutathione level were also estimated.

Results: BCAO followed by reperfusion produced a significant rise in cerebral infarct size, memory impairment and motor incoordination. Further a rise in acetylcholinesterase activity and TBARS level along with fall in brain nitrite/nitrate and glutathione levels was also noted. iPoCo consisting of three episodes of 10 s carotid artery occlusion and reperfusion (instituted immediately after BCAO) significantly attenuated infarct size, memory impairment, motor incoordination as well as altered biochemicals. iPoCo-induced neuroprotective effects were significantly abolished by pretreatment of L-NAME, a nonselective NOS inhibitor.

Conclusion: It may be concluded that the nitric oxide pathway probably plays a vital role in the neuroprotective mechanism of iPoCo.

No MeSH data available.


Related in: MedlinePlus