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抗氧化剂枸杞和抗坏血酸对大鼠肝脏再灌注损伤的影响。

Effects of the antioxidants lycium barbarum and ascorbic acid on reperfusion liver injury in rats.

作者信息

Wang N T, Lin H I, Yeh D Y, Chou T Y, Chen C F, Leu F C, Wang D, Hu R T

机构信息

Department of Medicine, Weigong Memorial Hospital, Miouli County, Taiwan.

出版信息

Transplant Proc. 2009 Dec;41(10):4110-3. doi: 10.1016/j.transproceed.2009.08.051.

Abstract

OBJECTIVE

Ischemia/reperfusion (I/R) of the rat liver can induce liver injury through mechanisms involving oxidative and nitrosative stresses. In this study we examined the effects of antioxidants Lycium barbarum (LB) and ascorbic acid on I/R-induced liver injury in rats.

METHODS

Liver ischemia was induced by clamping the common hepatic artery and portal vein of rats for 40 minutes. Thereafter, flow was restored with reperfusion for 90 minutes. Blood samples collected before ischemia and after reperfusion were analyzed for alanine transaminase (ALT), lactic dehydrogenase (LDH), hydroxyl radical, and nitric oxide (NO) levels. Pharmacologic interventions included administration of ascorbic acid (100 mg/kg, i.p., 1 hour before I/R) or LB, an extract of Gogi berries: 600 mg in 100 mL of drinking water for 2 weeks prior to experimentation.

RESULTS

This protocol resulted in elevation of blood concentrations of NO, hydroxyl radical, ALT, and LDH (P < .001) in the I/R-induced liver injury group. Ascorbic acid significantly attenuated the reperfusion liver injury by attenuating hydroxyl radical (P < .01) and NO (P < .05) release. The LB aggravated I/R-induced liver injury by increasing hydroxyl radical release with no effect on NO release.

DISCUSSION AND CONCLUSIONS

This I/R protocol resulted in oxidative and nitrosative stress and liver injury. Ascorbic acid showed significant protective effects on reperfusion liver injury by attenuating hydroxyl radical and NO release. In contrast, LB aggravated liver injury by increasing hydroxyl radical release.

摘要

目的

大鼠肝脏缺血/再灌注(I/R)可通过涉及氧化应激和亚硝化应激的机制诱导肝损伤。在本研究中,我们检测了抗氧化剂枸杞(LB)和抗坏血酸对I/R诱导的大鼠肝损伤的影响。

方法

通过夹闭大鼠肝总动脉和门静脉40分钟诱导肝脏缺血。此后,恢复血流再灌注90分钟。分析缺血前和再灌注后采集的血样中的丙氨酸转氨酶(ALT)、乳酸脱氢酶(LDH)、羟自由基和一氧化氮(NO)水平。药物干预包括给予抗坏血酸(100mg/kg,腹腔注射,在I/R前1小时)或枸杞提取物LB:在实验前2周,将600mg LB溶于100mL饮用水中。

结果

该方案导致I/R诱导的肝损伤组血液中NO、羟自由基、ALT和LDH浓度升高(P<.001)。抗坏血酸通过减弱羟自由基(P<.01)和NO(P<.05)释放,显著减轻再灌注肝损伤。LB通过增加羟自由基释放加重I/R诱导的肝损伤,而对NO释放无影响。

讨论与结论

该I/R方案导致氧化应激、亚硝化应激和肝损伤。抗坏血酸通过减弱羟自由基和NO释放,对再灌注肝损伤显示出显著的保护作用。相反,LB通过增加羟自由基释放加重肝损伤。

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