title: Calcium antagonist prevents calcium flux induced necrosis and apoptosis in ischemic reperfusion of rat liver.
abstract: Ca(2+) accumulation in mitochondria is responsible for the cell abnormality associated with ischemia and reperfusion injury. The present study was aimed to evaluate the efficacy of Ca(2+) channel blocker- amlodipine on the mitochondrial Ca(2+) accumulation in ischemic and reperfusion (I/R) induced liver injury. Eighteen wistar rats were divided in sham-operated control group-I (n = 6), ischemia and reperfusion group-II (n = 6) and amlodipine treated group-III (1 mg/kg body weight /daily by oral route for 7 days before induced ischemia reperfusion manouver) (n = 6). Rats were subjected to 1h of hepatic ischemia followed by 3 h reperfusion. Mitochondrial Ca(2+) content was measured and damage of mitochondria was confirmed by transmission electron microscopic examination. Bcl-2 gene expression was measured by reverse transcriptase polymerase chain reaction method. Pretreatment with Amlodipine effectively counteracted the alternation in mitochondrial Ca(2+) content. TEM and expression of Bcl-2 protein confirms the restoration of cellular normalcy and accredits the cytoprotective role of Amlodipine against I/R induced hepatic injury. These findings showed that the mechanism of regulation of Bcl-2 gene expression by amlodipine may be the inhibitory action of Ca(2+) entry into mitochondria and prevent apoptosis and necrosis.
authors.affiliation: Cellular and Microbiology Laboratory, College of Pharmacy, IFTM, Moradabad, 244001 U.P. India  ; Birla Institute of Technology and Sciences, Pilani, India.
authors.forename: Pronobesh
authors.initials: P
authors.lastname: Chattopadhyay
authors.forename: Nevneet
authors.initials: N
authors.lastname: Verma
authors.forename: Anurag
authors.initials: A
authors.lastname: Verma
authors.forename: Gunjan
authors.initials: G
authors.lastname: Shukla
authors.forename: Arun Kumar
authors.initials: AK
authors.lastname: Wahi
keywords: Amlodipine; Calcium channel blocker; Ischemic and reperfusion injury