中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
11期
2715-2717
,共3页
李文澜%夏中元%孙倩%赵博%江莹%詹丽英
李文瀾%夏中元%孫倩%趙博%江瑩%詹麗英
리문란%하중원%손천%조박%강형%첨려영
人参皂苷Rb1%急性肾损伤%肠缺血%再灌注损伤%NF-E2相关因子2%血红素氧合酶-1
人參皂苷Rb1%急性腎損傷%腸缺血%再灌註損傷%NF-E2相關因子2%血紅素氧閤酶-1
인삼조감Rb1%급성신손상%장결혈%재관주손상%NF-E2상관인자2%혈홍소양합매-1
Ginsenoside Rb1%Acute renal injury%Intestinal ischemia%Reperfusion injury%NF-E2-related factor-2%Heme oxygenase-1
目的 观察人参皂苷Rb1对肠缺血再灌注致肾损伤的影响及机制.方法 将48只成年雄性C57BL/6J小鼠随机分为4组(n=12):假手术组(S组)、肠缺血再灌注组(ⅡR组)、Rb1低剂量组(Rb1-30组)、Rb1高剂量组(Rb1-60组).采用小鼠肠缺血再灌注模型.Rb1-30组和Rb1-60组分别于再灌注前腹腔给予30、60 mg/kg的Rb1.再灌注2h时心脏采血检测血尿素氮(BUN)、肌酐(Cr)和中性粒细胞明胶酶相关脂质运载蛋白(NGAL),观察肾脏病理学改变,检测肾组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及Western blot检测血红素氧合酶-1(HO-1)、NF-E2相关因子(Nrf2)蛋白表达.结果 ⅢR组(HO-1:4.03±0.60,Nrf2:3.42 ±0.47)高于S组(HO-1:1.50±0.16,Nrf2:0.61 ±0.14)(P＜0.01),而Rh1-30组(HO-1:8.78±1.12,Nrf2:6.02±0.55)和Rb1-60组(HO-1:15.76±1.33,Nrf2:8.29±0.66)较ⅢR组进一步增高(P＜0.05).与S组(16.70 ±4.06)比较,ⅡR组(198.60±9.71)中肾损伤程度增高(P＜0.01),血清BUN(21.55±1.50)、Cr(20.65±1.53)和NGAL(155.93±8.07)水平、肾组织MDA(5.00±1.53)含量升高而SOD(9.49±1.39)活性降低(P＜0.01).与ⅡR组比较,Rb1-60组(94.60±9.24)中肾损伤程度减轻(P＜0.05),BUN(Rb1-30:15.52±1.23;Rb1-60:12.91±1.41)、Cr(Rb1-30: 16.00±1.50;Rb1-60: 13.14±1.22)和NGAL(Rb1-30:124.44±6.52;Rb1-60:101.76±12.20)水平、肾组织MDA(Rb1-30:4.12±0.47;Rb1-60:3.22±0.54)含量降低而SOD(Rb1-30:14.77±1.87;Rb1-60:18.91±1.56)活性升高(P＜0.01).结论 肠缺血再灌注可致肾损伤,人参皂苷Rb1通过激活Nrf2/ARE通路,诱导HO-1表达,从而减轻肠缺血再灌注所致肾损伤.
目的 觀察人參皂苷Rb1對腸缺血再灌註緻腎損傷的影響及機製.方法 將48隻成年雄性C57BL/6J小鼠隨機分為4組(n=12):假手術組(S組)、腸缺血再灌註組(ⅡR組)、Rb1低劑量組(Rb1-30組)、Rb1高劑量組(Rb1-60組).採用小鼠腸缺血再灌註模型.Rb1-30組和Rb1-60組分彆于再灌註前腹腔給予30、60 mg/kg的Rb1.再灌註2h時心髒採血檢測血尿素氮(BUN)、肌酐(Cr)和中性粒細胞明膠酶相關脂質運載蛋白(NGAL),觀察腎髒病理學改變,檢測腎組織超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及Western blot檢測血紅素氧閤酶-1(HO-1)、NF-E2相關因子(Nrf2)蛋白錶達.結果 ⅢR組(HO-1:4.03±0.60,Nrf2:3.42 ±0.47)高于S組(HO-1:1.50±0.16,Nrf2:0.61 ±0.14)(P＜0.01),而Rh1-30組(HO-1:8.78±1.12,Nrf2:6.02±0.55)和Rb1-60組(HO-1:15.76±1.33,Nrf2:8.29±0.66)較ⅢR組進一步增高(P＜0.05).與S組(16.70 ±4.06)比較,ⅡR組(198.60±9.71)中腎損傷程度增高(P＜0.01),血清BUN(21.55±1.50)、Cr(20.65±1.53)和NGAL(155.93±8.07)水平、腎組織MDA(5.00±1.53)含量升高而SOD(9.49±1.39)活性降低(P＜0.01).與ⅡR組比較,Rb1-60組(94.60±9.24)中腎損傷程度減輕(P＜0.05),BUN(Rb1-30:15.52±1.23;Rb1-60:12.91±1.41)、Cr(Rb1-30: 16.00±1.50;Rb1-60: 13.14±1.22)和NGAL(Rb1-30:124.44±6.52;Rb1-60:101.76±12.20)水平、腎組織MDA(Rb1-30:4.12±0.47;Rb1-60:3.22±0.54)含量降低而SOD(Rb1-30:14.77±1.87;Rb1-60:18.91±1.56)活性升高(P＜0.01).結論 腸缺血再灌註可緻腎損傷,人參皂苷Rb1通過激活Nrf2/ARE通路,誘導HO-1錶達,從而減輕腸缺血再灌註所緻腎損傷.
목적 관찰인삼조감Rb1대장결혈재관주치신손상적영향급궤제.방법 장48지성년웅성C57BL/6J소서수궤분위4조(n=12):가수술조(S조)、장결혈재관주조(ⅡR조)、Rb1저제량조(Rb1-30조)、Rb1고제량조(Rb1-60조).채용소서장결혈재관주모형.Rb1-30조화Rb1-60조분별우재관주전복강급여30、60 mg/kg적Rb1.재관주2h시심장채혈검측혈뇨소담(BUN)、기항(Cr)화중성립세포명효매상관지질운재단백(NGAL),관찰신장병이학개변,검측신조직초양화물기화매(SOD)활성、병이철(MDA)함량급Western blot검측혈홍소양합매-1(HO-1)、NF-E2상관인자(Nrf2)단백표체.결과 ⅢR조(HO-1:4.03±0.60,Nrf2:3.42 ±0.47)고우S조(HO-1:1.50±0.16,Nrf2:0.61 ±0.14)(P＜0.01),이Rh1-30조(HO-1:8.78±1.12,Nrf2:6.02±0.55)화Rb1-60조(HO-1:15.76±1.33,Nrf2:8.29±0.66)교ⅢR조진일보증고(P＜0.05).여S조(16.70 ±4.06)비교,ⅡR조(198.60±9.71)중신손상정도증고(P＜0.01),혈청BUN(21.55±1.50)、Cr(20.65±1.53)화NGAL(155.93±8.07)수평、신조직MDA(5.00±1.53)함량승고이SOD(9.49±1.39)활성강저(P＜0.01).여ⅡR조비교,Rb1-60조(94.60±9.24)중신손상정도감경(P＜0.05),BUN(Rb1-30:15.52±1.23;Rb1-60:12.91±1.41)、Cr(Rb1-30: 16.00±1.50;Rb1-60: 13.14±1.22)화NGAL(Rb1-30:124.44±6.52;Rb1-60:101.76±12.20)수평、신조직MDA(Rb1-30:4.12±0.47;Rb1-60:3.22±0.54)함량강저이SOD(Rb1-30:14.77±1.87;Rb1-60:18.91±1.56)활성승고(P＜0.01).결론 장결혈재관주가치신손상,인삼조감Rb1통과격활Nrf2/ARE통로,유도HO-1표체,종이감경장결혈재관주소치신손상.
Objective To investigate the effects of ginsenoside Rb1 on acute renal injury induced by intestinal ischemia reperfusion (ⅡR) in mice.Methods Forty-eight male C57BL/6J mice were randomly divided into four groups (n =12) : sham group, IIR group, 30 mg/kg ginsenoside Rb1 (Rb1-30) group, and 60 mg/kg ginsenoside Rb1 (Rb1-60) group.Intestinal ischemia reperfusion model in mice was established.30 mg/kg and 60 mg/kg ginsenoside Rb1 were given intraperitoneally in Rb1-30 group and Rb1-60 group respectively before reperfusion.After 2 h reperfusion, blood urea nitrogen (BUN), creatinine (Cr), and neutrophil gelatinase associated lipocalin (NGAL) levels in serum were measured.Renal histological changes were observed and evaluated.Superoxide dismutase (SOD) and malondialdehyde (MDA) levels in renal tissues were detected.Western blotting was used to observe the expression levels of NF and E2 related factor (Nrf2) and heme oxygenase-1 (HO-1) in renal tissues.Results The expression levels of HO-1 and Nrf2 in ⅡR group (4.03 ±0.60 and 2:3.42 ±0.47) were significantly higher than those in S group (1.50 ±0.16 and 2:0.61 ±0.14) (P＜0.01), and those in RB-30 group (8.78 ± 1.12 and 2:6.02 ±0.55) and RB-60 group (15.76 ± 1.33 and 8.29 ±0.66) were significantly higher than those in ⅡR group (P ＜0.05).ⅡR-induced renal injury in ⅡR group (198.60 ± 9.71) was significantly aggravated as compared with S group (16.70 ±4.06) (P ＜0.01).In ⅡR group, BUN (21.55 ±1.50) , Cr (20.65 ± 1.53) and NGAL (155.93 ±8.07) in serum and MDA (5.00 ± 1.53, P ＜0.01) in the renal tissues were increased and SOD (9.49 ± 1.39) decreased (P ＜ 0.01) as compared with S group.Ginsenoside Rb1 (30, 60 mg/kg) could alleviate renal injury (Rb1-30: 135.10±8.71;Rb1-60: 94.60 ±9.24, P＜0.01), decrease BUN (Rb1-30:15.52 ± 1.23;Rb1-60:12.91 ±1.41), Cr (Rb1-30: 16.00±1.50;Rb1-60: 13.14±1.22) and NGAL (Rb1-30: 124.44±6.52;Rb1-60:101.76 ± 12.20) in serum, MDA level (Rb1-30: 4.12 ±0.47;Rb1-60: 3.22 ±0.54) (P ＜0.01) in the renal tissues, and increase SOD level (Rb1-30: 14.77 ± 1.87;Rb1-60: 18.91 ± 1.56) (P ＜0.01).Conclusion Ginsenoside Rb1 attenuated acute renal injury induced by IIR by activating Nrf2/ARE pathway and upregulating the protein expression of HO-1.
