AIM: To investigate the effect of sulforaphane (SFN) on regulation of NF-E2-related factor-2 (Nrf2)-antiox-idant response element (ARE) pathway in liver injury induced by intestinal ischemia/reperfusion (I/R). METHODS...AIM: To investigate the effect of sulforaphane (SFN) on regulation of NF-E2-related factor-2 (Nrf2)-antiox-idant response element (ARE) pathway in liver injury induced by intestinal ischemia/reperfusion (I/R). METHODS: Rats were divided randomly into four ex-perimental groups: control, SFN control, intestinal I/R and SFN pretreatment groups (n = 8 in each group). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h and 2 h reperfu-sion. In the SFN pretreatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg SFN 1 h before the op-eration. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured. Liver tissue superoxide dismutase (SOD), myeloperoxidase (MPO), glutathione (GSH) and glutathione peroxidase (GSH-Px) activity were assayed. The liver transcription factor Nrf2 and heme oxygenase-1 (HO-1) were determined by immunohistochemical analysis and Western blotting analysis.RESULTS: Intestinal I/R induced intestinal and liver injury, characterized by histological changes as well as a signif icant increase in serum AST and ALT levels (AST: 260.13 ± 40.17 U/L vs 186.00 ± 24.21 U/L, P < 0.01; ALT: 139.63 ± 11.35 U/L vs 48.38 ± 10.73 U/L, P < 0.01), all of which were reduced by pretreatment with SFN, respectively (AST: 260.13 ± 40.17 U/L vs 216.63 ± 22.65 U/L, P < 0.05; ALT: 139.63 ± 11.35 U/L vs 97.63 ± 15.56 U/L, P < 0.01). The activity of SOD in the liver tissue decreased after intestinal I/R (P < 0.01), which was enhanced by SFN pretreatment (P < 0.05). In ad-dition, compared with the control group, SFN markedly reduced liver tissue MPO activity (P < 0.05) and elevat-ed liver tissue GSH and GSH-Px activity (P < 0.05, P < 0.05), which was in parallel with the increased level of liver Nrf2 and HO-1 expression.CONCLUSION: SFN pretreatment attenuates liver injury induced by intestinal I/R in rats, attributable to the antioxidant effect through Nrf2-ARE pathway.展开更多
目的探讨黄芩茎叶总黄酮(Scutellaria baiculensis stem-leaf total flavonoid,SSTF)对大鼠心肌缺血再灌注损伤的保护作用。方法40只SD大鼠随机分为假手术组、缺血再灌注组和SSTF预处理组。SSTF组大鼠于术前1周分别灌胃不同剂量的SSTF〔...目的探讨黄芩茎叶总黄酮(Scutellaria baiculensis stem-leaf total flavonoid,SSTF)对大鼠心肌缺血再灌注损伤的保护作用。方法40只SD大鼠随机分为假手术组、缺血再灌注组和SSTF预处理组。SSTF组大鼠于术前1周分别灌胃不同剂量的SSTF〔(17.5、35、70mg/(kg.d)〕,另两组给等量生理盐水。采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注模型。缺血30min、再灌注2h后,观察大鼠心电图的变化;并用免疫组织化学法检测心肌组织中Bax和Bcl-2蛋白表达情况。结果SSTF抑制了缺血再灌注损伤大鼠心电图T波升高,降低了心律失常发生率。缺血再灌注组Bcl-2蛋白表达阳性细胞率明显比假手术组低(P<0.05),Bax蛋白表达阳性细胞率明显较假手术组高,而SSTF预处理组Bcl-2蛋白表达阳性细胞率明显高于缺血再灌注组(P<0.05),Bax蛋白表达阳性细胞率明显较缺血再灌注组为低(P<0.05)。结论SSTF预处理对缺血再灌注的心肌细胞具有保护作用,其机制可能与上调Bcl-2和下调Bax蛋白表达进而抑制心肌细胞凋亡有关。展开更多
基金Supported by The grants of Chinese National Natural Science Foundation, No. 30872449the grants of the Dalian Scientific Research Foundation, No. 2008E13SF217
文摘AIM: To investigate the effect of sulforaphane (SFN) on regulation of NF-E2-related factor-2 (Nrf2)-antiox-idant response element (ARE) pathway in liver injury induced by intestinal ischemia/reperfusion (I/R). METHODS: Rats were divided randomly into four ex-perimental groups: control, SFN control, intestinal I/R and SFN pretreatment groups (n = 8 in each group). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h and 2 h reperfu-sion. In the SFN pretreatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg SFN 1 h before the op-eration. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured. Liver tissue superoxide dismutase (SOD), myeloperoxidase (MPO), glutathione (GSH) and glutathione peroxidase (GSH-Px) activity were assayed. The liver transcription factor Nrf2 and heme oxygenase-1 (HO-1) were determined by immunohistochemical analysis and Western blotting analysis.RESULTS: Intestinal I/R induced intestinal and liver injury, characterized by histological changes as well as a signif icant increase in serum AST and ALT levels (AST: 260.13 ± 40.17 U/L vs 186.00 ± 24.21 U/L, P < 0.01; ALT: 139.63 ± 11.35 U/L vs 48.38 ± 10.73 U/L, P < 0.01), all of which were reduced by pretreatment with SFN, respectively (AST: 260.13 ± 40.17 U/L vs 216.63 ± 22.65 U/L, P < 0.05; ALT: 139.63 ± 11.35 U/L vs 97.63 ± 15.56 U/L, P < 0.01). The activity of SOD in the liver tissue decreased after intestinal I/R (P < 0.01), which was enhanced by SFN pretreatment (P < 0.05). In ad-dition, compared with the control group, SFN markedly reduced liver tissue MPO activity (P < 0.05) and elevat-ed liver tissue GSH and GSH-Px activity (P < 0.05, P < 0.05), which was in parallel with the increased level of liver Nrf2 and HO-1 expression.CONCLUSION: SFN pretreatment attenuates liver injury induced by intestinal I/R in rats, attributable to the antioxidant effect through Nrf2-ARE pathway.
文摘目的探讨黄芩茎叶总黄酮(Scutellaria baiculensis stem-leaf total flavonoid,SSTF)对大鼠心肌缺血再灌注损伤的保护作用。方法40只SD大鼠随机分为假手术组、缺血再灌注组和SSTF预处理组。SSTF组大鼠于术前1周分别灌胃不同剂量的SSTF〔(17.5、35、70mg/(kg.d)〕,另两组给等量生理盐水。采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注模型。缺血30min、再灌注2h后,观察大鼠心电图的变化;并用免疫组织化学法检测心肌组织中Bax和Bcl-2蛋白表达情况。结果SSTF抑制了缺血再灌注损伤大鼠心电图T波升高,降低了心律失常发生率。缺血再灌注组Bcl-2蛋白表达阳性细胞率明显比假手术组低(P<0.05),Bax蛋白表达阳性细胞率明显较假手术组高,而SSTF预处理组Bcl-2蛋白表达阳性细胞率明显高于缺血再灌注组(P<0.05),Bax蛋白表达阳性细胞率明显较缺血再灌注组为低(P<0.05)。结论SSTF预处理对缺血再灌注的心肌细胞具有保护作用,其机制可能与上调Bcl-2和下调Bax蛋白表达进而抑制心肌细胞凋亡有关。