中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2015年
2期
169-173
,共5页
王俊%张珍%邵加庆%蒋卫民%顾萍%江时森
王俊%張珍%邵加慶%蔣衛民%顧萍%江時森
왕준%장진%소가경%장위민%고평%강시삼
糖尿病%血脂康%胰岛分泌功能%氧化应激
糖尿病%血脂康%胰島分泌功能%氧化應激
당뇨병%혈지강%이도분비공능%양화응격
Diabetes mellitus%Xuezhikang%Islet endocrine function%Oxidative stress
目的:探讨血脂康对db/db糖尿病小鼠胰岛分泌功能和氧化应激(OS)的影响。方法选取db/db小鼠40只,随机分为血脂康组和db/db组,各20只,另选取db/m小鼠20只作为对照(NC)组,分别给予血脂康和安慰剂灌胃。每周监测代谢指标,8周后行腹腔葡萄糖耐量试验(IPGTT),离体胰岛灌流评价胰岛分泌功能,免疫组织化学法分析胰岛内8‐羟‐2c‐脱氧鸟苷(8‐OHdG),4‐羟壬烯醛(4‐HNE)和gp91phox的表达水平。结果干预8周后,血脂康组FPG和FIns均低于db/db组[FPG:(18.4±3.4)vs(25.9±2.2)mmol/L;FIns:(7.7±0.8)vs(9.8±1.4)mIU/L,P<0.05]。IPGTT糖负荷后各时间点,血脂康组葡萄糖曲线下面积(AUCg)均低于db/db组[(1800.7±187.1)vs(2550.0±179.6),P<0.05],而胰岛素曲线下面积(AUCi)显示,30min时AUCi0~30高于db/db组[(285.3±8.9)vs(268.5±10.4),P<0.05]。与db/db组比较,血脂康组在给予16.7mm高糖刺激1min后胰岛素分泌升高。免疫组织化学法显示,与db/db组比较,血脂康组胰岛内8‐OhdG,4‐HNE和gp91phox的表达降低更明显(P<0.05)。结论血脂康能降低胰岛OS反应,并改善葡萄糖代谢。
目的:探討血脂康對db/db糖尿病小鼠胰島分泌功能和氧化應激(OS)的影響。方法選取db/db小鼠40隻,隨機分為血脂康組和db/db組,各20隻,另選取db/m小鼠20隻作為對照(NC)組,分彆給予血脂康和安慰劑灌胃。每週鑑測代謝指標,8週後行腹腔葡萄糖耐量試驗(IPGTT),離體胰島灌流評價胰島分泌功能,免疫組織化學法分析胰島內8‐羥‐2c‐脫氧鳥苷(8‐OHdG),4‐羥壬烯醛(4‐HNE)和gp91phox的錶達水平。結果榦預8週後,血脂康組FPG和FIns均低于db/db組[FPG:(18.4±3.4)vs(25.9±2.2)mmol/L;FIns:(7.7±0.8)vs(9.8±1.4)mIU/L,P<0.05]。IPGTT糖負荷後各時間點,血脂康組葡萄糖麯線下麵積(AUCg)均低于db/db組[(1800.7±187.1)vs(2550.0±179.6),P<0.05],而胰島素麯線下麵積(AUCi)顯示,30min時AUCi0~30高于db/db組[(285.3±8.9)vs(268.5±10.4),P<0.05]。與db/db組比較,血脂康組在給予16.7mm高糖刺激1min後胰島素分泌升高。免疫組織化學法顯示,與db/db組比較,血脂康組胰島內8‐OhdG,4‐HNE和gp91phox的錶達降低更明顯(P<0.05)。結論血脂康能降低胰島OS反應,併改善葡萄糖代謝。
목적:탐토혈지강대db/db당뇨병소서이도분비공능화양화응격(OS)적영향。방법선취db/db소서40지,수궤분위혈지강조화db/db조,각20지,령선취db/m소서20지작위대조(NC)조,분별급여혈지강화안위제관위。매주감측대사지표,8주후행복강포도당내량시험(IPGTT),리체이도관류평개이도분비공능,면역조직화학법분석이도내8‐간‐2c‐탈양조감(8‐OHdG),4‐간임희철(4‐HNE)화gp91phox적표체수평。결과간예8주후,혈지강조FPG화FIns균저우db/db조[FPG:(18.4±3.4)vs(25.9±2.2)mmol/L;FIns:(7.7±0.8)vs(9.8±1.4)mIU/L,P<0.05]。IPGTT당부하후각시간점,혈지강조포도당곡선하면적(AUCg)균저우db/db조[(1800.7±187.1)vs(2550.0±179.6),P<0.05],이이도소곡선하면적(AUCi)현시,30min시AUCi0~30고우db/db조[(285.3±8.9)vs(268.5±10.4),P<0.05]。여db/db조비교,혈지강조재급여16.7mm고당자격1min후이도소분비승고。면역조직화학법현시,여db/db조비교,혈지강조이도내8‐OhdG,4‐HNE화gp91phox적표체강저경명현(P<0.05)。결론혈지강능강저이도OS반응,병개선포도당대사。
Objective To investigate the effects of Xuezhikang on pancreatic islet endocrine function and local oxidative stress in db/db diabetic mice. Methods A total of 40 male genetically diabetic C57BL/KsJ‐db/db mice were randomly assigned into xuezhikang group treated with xuezhikang at 300 mg/(kg?d) and db/db group treated with placebo.In addition ,another 20 age‐matched lean non‐diabetic C57BL/KsJ‐db/m littermates served as normal control (NC) group. The metabolic indexes were measured every week. After 8 week ,10 mice were randomly selected from each group and received intraperitoneal glucose tolerance test (IPGTT).The in vitro insulin release kinetics was evaluated by perifusion system and the expression levels of gp91phox ,8‐OhdG and 4‐HNE were analyzed by immunohistochemical method. Results After 8 week treatment ,FPG and FIns were lower in Xuezhikang group than in db/db group[FPG :(18.4 ± 3.4) vs (25.9 ± 2.2) mmol/L ;FIns :(7.7 ± 0.8) vs (9.8 ± 1.4) mIU/L ,P<0.05] . At the various time points after IPGTT ,the AUCg was lower in Xuezhikang group than in db/db group [(1800.7±187.1) vs (2550.4±179.6),P< 0.05],and at the 30 minute after IPGTT ,the AUCi was higher in Xuezhikang group than in db/db group[(285.3 ± 8.9) vs (268.5 ± 10.4) ,P<0.05].Compared with the db/db group ,since 1 minute point after high‐concentration glucose stimulation ,the insulin level increased remarkably in Xuezhikang group.Immunohistochemistry method showed that compared with db/db group ,xuezhikang group showed the expression of gp91phox ,8‐OhdG and 4‐HNE was reduced (P<0.05). Conclusion Xuezhikang can inhibit the local oxidative stress of pancreatic islet and improve glucose metabolism in db/db diabetic mice.