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AIM:To investigate the chemopreventive effects of 1α,25-dihydroxyvitamin D_3 in diethylnitrosamine induced,phenobarbital promoted rat hepatocarcinogenesis.METHODS:The rats were randomly divided into 6 differentgroups (A-F).Groups A,C and E rats received a singleintraperitoneal (i.p) injection of diethylnitrosamine (DEN)at a dose of 200mg/kg body mass in 9g/L NaCl solution at4 wk of age,while group B served as normal vehicle controlreceived normal saline once.After a brief recovery of 2 wk,all the DEN treated rats were given phenobarbital (PB) at0.5g/L daily in the basal diet till wk 20.Group A was DENcontrol.Treatment of 1α,25-(OH)_2D_3 in group C was started4 wk prior to DEN injection and continued thereafter till wk20 at a dose of 0.3μg/100μL propylene glycol per onesingle dose (os) twice a week.Group E received thetreatment of 1α,25-(OH)_2D_3 at the same dose mentionedas above for 15 wk.The rats in group D and F received 1α,25-(OH)_2D_3 alone as in group C without DEN injection.RESULTS:The comet assay showed statistically highermean values for length to width ratios (L:W) of DNA massand tailed cells (P<0.01;P<0.01 respectively) in DEN treatedrats as compared to their normal controls.Continuoussupplementation of 1α,25-dihydroxyvitaminD_3 showed asignificant (P<0.01) decrease in L:W ratio of DNA masstailed cells.Furthermore,1α,25-(OH)_2D_3 supplementationselevated the super oxide dismutase (SOD) activity,hepaticmalondialdehyde (MDA) level,reduced glutathione (GSH)and glutathione S-transferase (GST) activity (P<0.01,P<0.05,P<0.05 and P<0.05 respectively).As an endpointmarker histological changes were observed to establishthe chemopreventive effects of 1α,25-dihydroxyvitaminD_3.CONCLUSION:Supplementations of 1α,25-(OH)_2D_3 has a marked protection against hepatic nodulogenesis,antioxidant enzymes and DNA damages in DEN induced rathepatocarcinogenesis promoted by phenobarbital.
AIM: To investigate the chemopreventive effects of 1α, 25-dihydroxyvitamin D_3 in diethylnitrosamine induced, phenobarbital promoted rat hepatocarcinogenesis. METHODS: The rats were randomly divided into 6 different groups (AF) .Groups A, C and E rats were received a single in traititoneal (ip) injection of diethylnitrosamine (DEN) at a dose of 200 mg / kg body mass in 9 g / L NaCl solution at 4 wk of age, while group B served as normal vehicle controlreceived normal saline once. After a brief recovery of 2 wk, all the DEN treated Rats were given phenobarbital (PB) at 0.5 g / L daily in the basal diet till wk 20. Group A was DEN control. Treatment of 1α, 25- (OH) _2D_3 in group C was started4 wk prior to DEN injection and the subsequent meal wk20 at a dose of 0.3 μg / 100 μL propylene glycol per onesingle dose (os) twice a week. Group E received the treatment of 1α, 25- (OH) _2D_3 at the same dose mentionedas above for 15 wk. rats in group D and F received 1α, 25- (OH) _2D_3 alone as in group C without DEN injectio n.RESULTS: The comet assay showed pedigree higher values for length to width ratios (L: W) of DNA mass and tailed cells (P <0.01; P <0.01 respectively) in DEN treated rats as compared to their normal controls. Continuoussupplementation of 1α, 25-dihydroxyvitaminD_3 showed asignificant (P <0.01) decrease in L: W ratio of DNA masstailed cells. Frthermore, 1α, 25- (OH) _2D_3 supplementationselevated the super oxide dismutase (SOD) activity, hepaticmalondialdehyde (MDA) GSH) and glutathione S-transferase (GST) activity (P <0.01, P <0.05 and P <0.05 respectively) Supplementations of 1α, 25- (OH) _2D_3 has a marked protection against hepatic nodulogenesis, antioxidant enzymes and DNA damages in DEN induced rathepatocarcinogenesis promoted by phenobarbital.