Prabhat Singh, Bhupesh Sharma
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Prabhat Singh1, Bhupesh Sharma2,3*
1Ph.D Student, Neuropharmacology Lab., Department of Pharmacology, KSCP,
Subharti University, Meerut, Uttar Pradesh, India.
2Professor, Department of Pharmacology, Amity Institute of Pharmacy,
Amity University, Sector-125, Noida - 201313, Uttar Pradesh, India.
3Chief Consultant, CNS Pharmacology, Conscience Research, Pocket F- 233,
B (Near Sai Vatika), Dilshad Garden, Delhi - 110095 India.
Volume - 14,
Issue - 5,
Year - 2021
Cerebral ischemia and ischemia-reperfusion is an essential contributor to acute cerebral stroke. Ischemic preconditioning (IPC) has been proven to provide neuroprotection in ischemia-reperfusion injury in rats, but their mechanism behind neuroprotection in cerebral stroke are still unclear. Central histaminergic pathway has crucial role in the pathogenesis of cerebral stroke, but their neuroprotective role in IPC is still unidentified. This research explores the role of histamine-1 receptor in IPC induced neuroprotection against ischemia-reperfusion induced cerebral injury. Rat were subjected to 17 min of global cerebral ischemia (GCI) by occluding both carotid arteries followed by reperfusion for 24 h, to produce ischemia-reperfusion induced cerebral injury. TTC staining was used to measure cerebral infarct size. Morris water maze test was used to assess memory. Inclined beam-walk, hanging wire, lateral push and rota-rod tests were used to assess degree of motor incoordination. Brain acetylcholinesterase activity, nitrite/nitrate, glutathione, TBARS and MPO levels were also examined. GCI has produced a significant increase in cerebral infarction, brain nitrite/nitrate, MPO, TBARS and AChE activity along with a reduction in glutathione content. Impairment of memory and motor coordination were also noted in GCI induced rat. IPC was employed that consist of 3 preceding episodes of ischemia (1 min) and reperfusion (1 min) both immediately before GCI significantly decreased cerebral infarction, motor incoordination, memory impairment and biochemical impairment. Pretreatment with L-histidine mimicked the neuroprotective effects of IPC. L-histidine induced neuroprotection were significantly abolished by chlorpheniramine, a H1 receptor antagonist. We conclude that neuroprotective effects of IPC, probably occurs through the central histaminergic pathway, and histamine-1 receptor could be a new target behind the neuroprotective mechanism of IPC.
Cite this article:
Prabhat Singh, Bhupesh Sharma. Pharmacological connection of Histamine-1 (H1) Receptor Mediated Neuroprotective mechanism of Ischemic preconditioning in rat.Research Journal of Pharmacy and Technology. 2021; 14(5):2717-2. doi: 10.52711/0974-360X.2021.00479
Prabhat Singh, Bhupesh Sharma. Pharmacological connection of Histamine-1 (H1) Receptor Mediated Neuroprotective mechanism of Ischemic preconditioning in rat.Research Journal of Pharmacy and Technology. 2021; 14(5):2717-2. doi: 10.52711/0974-360X.2021.00479 Available on: https://rjptonline.org/AbstractView.aspx?PID=2021-14-5-63
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