论文部分内容阅读
AIM:To investigate the role of nitric oxide(NO)in Toll-like receptor 2(TLR2)/4mRNA expression in livers ofacute hemorrhagic necrotizing pancreatitis(AHNP)rats.METHODS:One hundred and ten SD male rats wererandomly divided into sham-operated group(n=10),AHNP group(n=30),chloroquine(CQ)-treated group(n=30)and L-Arg-treated group(n=40).TLR2/4mRNAexpression in the liver of AHNP rats was measured byRT-PCR.RESULTS:Expression of TLR2/4mRNA could bedetected in the liver of AHNP rats in sham-operatedgroup(0.155E-5+0.230E-6 and 0.115E-2±0.545E-4),but was markedly increased at 3 h in AHNP group(0.197E-2±0.114E-3 and 0.175±0.349E-2)peakingat 12 h(0.294E-2±0.998E-4 and 2.673±2.795E-2,P<0.01).Hepatic injuries were aggravated,TNF-αconcentration in the liver was increased and NOconcentration was decreased(P<0.05 or P<0.01).When TLR2/4mRNA expression was inhibited by CQ(3h:1.037E-4±3.299E-6 and 0.026±3.462E-3;6 h:1.884E-4±4.679E-6 and 0.108±6.115E-3;12 h:2.443E-4±7.714E-6 and 0.348±6.807E-3;P<0.01),hepatic injuries were relieved,NO concentration inthe liver was increased and TNF-α concentration wasdecreased(P<0.05 or P<0.01).When rats with AHNP were treated with L-Arg,TLR2/4mRNA expressionin the liver could be effectively inhibited(50 mg-T:0.232E-2±0.532E-4 and 0.230±6.883E-3;100 mg-T:0.210E-2±1.691E-4 and 0.187±0.849E-2;200 mg-T:0.163E-2±0.404E-4 and 0.107±0.195E-2;400 mg-T:0.100E-2±0.317E-4 and 0.084±0.552E-2;P<0.01)and hepatic injuries were relieved.At the same time,NO concentration in the liver was markedly increasedand TNF-α concentration was decreased(P<0.05 orP<0.01).CONCLUSION:The expression of TLR2/4mRNA isincreased and hepatic injuries are aggravated in the liverof AHNP rats.TLR2/4mRNA gene expression in the liverof AHNP rats can be markedly inhibited by NO,leadingto the relief of hepatic injuries.
AIM: To investigate the role of nitric oxide (NO) in Toll-like receptor 2 (TLR2) / 4 mRNA expression in livers of acute hemorrhagic necrotizing pancreatitis (AHNP) rats. METHODS: One hundred and ten SD male rats were randomly divided into sham-operated (n = 10), AHNP group (n = 30), chloroquine (CQ) -treated group (n = 30) and L-Arg-treated group measured by RT-PCR .RESULTS: Expression of TLR2 / 4 mRNA could bedetected in the liver of AHNP rats in sham-operatedgroup (0.155E-5 + 0.230E-6 and 0.115E-2 ± 0.545E-4), but was markedly increased at 3 h in AHNP group (0.197E-2 ± 0.114E-3 and 0.175 ± 0.349E-2) peakingat 12 h (0.294E-2 ± 0.998E-4 and 2.673 ± 2.795E-2, P <0.01). Hepatic injuries were aggravated, TNF-αconcentration in the liver was increased and NOconcentration was decreased (P <0.05 or P <0.01) .When TLR2 / 4 mRNA expression was inhibited by CQ (3h: 1.037E-4 ± 3.299E-6 and 0.026 ± 3.462E-3; 6 h: 1.884E-4 ± 4.679E-6 and 0.108 ± 6.115E-3; 12 h: 2.443E-4 ± 7.714E-6 and 0.348 ± 6.807E-3; P <0.01), hepatic injuries were relieved, NO concentration inthe liver was increased and TNF-α concentration was decreased (P <0.05 or P <0.01) .When rats with AHNP were treated with L-Arg, TLR2 / 4 mRNA expressionin the liver could (50 mg-T: 0.232E-2 ± 0.532E-4 and 0.230 ± 6.883E-3; 100 mg-T: 0.210E-2 ± 1.691E-4 and 0.187 ± 0.849E-2; 200 mg -T: 0.163E-2 ± 0.404E-4 and 0.107 ± 0.195E-2; 400 mg-T: 0.100E-2 ± 0.317E-4 and 0.084 ± 0.552E-2; P <0.01) and hepatic injuries were relieved. At the same time, NO concentration in the liver was markedly increased and TNF-α concentration was decreased (P <0.05 or P <0.01). CONCLUSION: The expression of TLR2 / 4 mRNA is in- creased and hepatic injuries are aggravated in the liver of AHNP rats. TLR2 / 4 mRNA gene expression in the liver of AHNP rats can be markedly inhibited by NO, leadingto the relief of hepatic injuries.