Folic acid inhibits necrosis and apoptosis in ischemic and reperfusion induced injury in rat liver

다국어 초록 (Multilingual Abstract)

Temporary clamping of the portal triad is a common strategy to minimize bleeding during liver
transplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction of
oxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis and
necrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hour
reperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6),
ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/daily
by oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptotic
and necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury was
assessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology
and electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated by
increased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic and
necrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatment
with folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1
h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedly
diminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, which
reached a level comparable to saline-treated rat of sham operated group. On the basis of our
findings it may be concluded that folic acid afforded significant protection from necrosis and
apoptosis in I/R injury.

다국어 초록 (Multilingual Abstract)

Temporary clamping of the portal triad is a common strategy to minimize bleeding during liver
transplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction of
oxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis and
necrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hour
reperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6),
ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/daily
by oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptotic
and necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury was
assessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology
and electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated by
increased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic and
necrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatment
with folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1
h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedly
diminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, which
reached a level comparable to saline-treated rat of sham operated group. On the basis of our
findings it may be concluded that folic acid afforded significant protection from necrosis and
apoptosis in I/R injury.

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