Mechanism of action of glutamine in portal hypertensive gastropathy in rats
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摘要: 目的初步探讨谷氨酰胺在大鼠门静脉高压性胃病中的作用及相关机制。方法 60只SD大鼠随机均分为4组,A组(假手术)、B组(假手术组+谷氨酰胺)、C组(门静脉部分结扎)、D组(门静脉部分结扎+谷氨酰胺),每组15只。采用门静脉主干部分结扎法复制大鼠门静脉高压性胃病模型,2周后测量大鼠门静脉压力(PVP)、胃损伤指数(GI)、胃黏膜病理评分(PI)及肝脏形态变化,检测血浆中ALT、AST、Alb、一氧化氮(NO)、TNFα、超氧化物歧化酶(SOD)的表达情况。计量资料2组间比较采用t检验,多组间比较采用方差分析,进一步两两比较采用LSD-t检验。结果 4组间PVP比较差异有统计学差异[(1.17±0.15)k Pa vs(1.21±0.19)k Pa vs(2.65±0.16)k Pa vs(2.18±0.22)k Pa,F=4.60,P<0.05],C组、D组分别与A组、B组比较,差异均有统计学意义(P值均<0.05);C、D组GI和PI相比差异均有统计学意义[15.52±2.05 vs 8.26±1.23,7.56±1.53 vs 3.15±1.42,t值分别为5.84、7....
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关键词:
- 门静脉高压性胃病 /
- 谷氨酰胺 /
- 大鼠,Sprague-Dawley
Abstract: Objective To investigate the role and mechanism of action of glutamine in portal hypertension gastropathy ( PHG) in rats.Methods A total of 60 Sprague-Dawley rats were randomly divided into groups A ( sham-operation) , B ( sham-operation + glutamine) , C ( partial portal vein ligation) , and D ( partial portal vein ligation + glutamine) . A rat model of PHG was established by partial ligation of the main portal vein. Portal vein pressure ( PVP) , gastric injury index ( GI) , pathological integral ( PI) of the gastric mucosa, and liver morphological changes were measured after 2 weeks, and the plasma levels of alanine aminotransferase ( ALT) , aspartate aminotransferase ( AST) , albumin ( Alb) , nitric oxide ( NO) , tumor necrosis factor-α ( TNFα) , and superoxide dismutase ( SOD) were also measured. The t-test was used for comparison of continuous data between two groups, an analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results There was a significant difference in PVP between groups A, B, C, and D ( 1. 17 ± 0. 15 k Pa vs 1. 21 ± 0. 19 k Pa vs 2. 65 ± 0. 16 k Pa vs 2. 18 ± 0. 22 k Pa, F = 4. 60, P < 0. 05) , and there were also significant differences between groups C/D and groups A/B ( P < 0. 05) . There were significant differences between groups C and D in GI ( 15. 52 ± 2. 05 vs 8. 26 ± 1. 23, t = 5. 84, P < 0. 05) and PI ( 7. 56 ± 1. 53 vs 3. 15 ± 1. 42, t = 7. 45, P < 0. 05) . There were no significant differences in ALT, AST, and Alb between the four groups ( all P > 0. 05) . There were significant differences between the four groups in TNFα ( 0. 56 ± 0. 11 ng/ml vs 0. 41 ± 0. 21 ng/ml vs 1. 35 ± 0. 26 ng/ml vs 0. 68 ± 0. 21 ng/ml, F = 5. 24, P < 0. 05) , NO ( 1. 63 ± 0. 15 μmol/gpro vs 1. 41 ± 0. 12 μmol/gpro vs 5. 52 ± 1. 06 μmol/gpro vs 2. 26 ± 0. 83μmol/gpro, F = 8. 40, P < 0. 05) , and SOD ( 148. 21 ± 6. 21 U/mg vs 154. 21 ± 5. 31 U/mg vs 74. 56 ± 4. 21 U/mg vs 135. 25 ± 4. 82 U/mg, F = 14. 78, P < 0. 05) . There were significant differences in TNFα, NO, and SOD between group C and groups A/B ( all P <0. 05) , as well as between groups C and D ( all P < 0. 05) . Conclusion PHG has various pathogenic factors. Glutamine can alleviate gastric mucosal edema and hemorrhage in rats with PHG and reduce the content of NO, TNFα, and SOD. Glutamine has a good antioxidant effect and thus helps with the treatment of PHG.-
Key words:
- portal hypertensive gastropathy /
- glutamine /
- rats, sprague-dawley
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