泸州医学院学报
瀘州醫學院學報
로주의학원학보
JOURNAL OF LUZHOU MEDICAL COLLEGE
2015年
1期
1-6
,共6页
刘霜%徐勇%吕诗诗%罗巧彦
劉霜%徐勇%呂詩詩%囉巧彥
류상%서용%려시시%라교언
NLRP3%炎症小体%糖尿病肾病%棕榈酸%N-乙酰半胱氨酸
NLRP3%炎癥小體%糖尿病腎病%棕櫚痠%N-乙酰半胱氨痠
NLRP3%염증소체%당뇨병신병%종려산%N-을선반광안산
NLRP3%Inflammasome%Diabetic nephropathy%Palmitic acid%N-acetyl-L-cysteine
目的：：探讨NLRP3炎症小体在游离脂肪酸(free fatty acids, FFAs)诱导下的肾小球系膜细胞(HBZY-1)中的表达及氧化应激在其中的影响。方法：将HBZY-1细胞分为正常对照组、不同浓度棕榈酸组、高棕榈酸+N-乙酰半胱氨酸(N-acetyl-L-cysteine, NAC)组。各组细胞培养6、9、12 h后采用Western blotting和RT-PCR检测各组NLRP3、Caspase-1、IL-1β蛋白及mRNA表达,并同时观察NAC对各组蛋白及mRNA表达的影响。结果：棕榈酸刺激肾系膜细胞NLRP3炎症小体信号分子的表达变化：与对照组相比,不同作用浓度和时间的棕榈酸均可上调NLRP3、Caspase-1、IL-1β蛋白及mRNA表达(P<0.05),且呈浓度和时间依赖性。与单纯棕榈酸组相比, NAC预处理可阻止棕榈酸诱导的NLRP3、Caspase-1、IL-1β蛋白及mRNA表达上调(P<0.05)。结论：棕榈酸可通过氧化应激机制诱导系膜细胞NLRP3炎症小体信号的活化,参与糖尿病肾病炎症的发生。
目的：：探討NLRP3炎癥小體在遊離脂肪痠(free fatty acids, FFAs)誘導下的腎小毬繫膜細胞(HBZY-1)中的錶達及氧化應激在其中的影響。方法：將HBZY-1細胞分為正常對照組、不同濃度棕櫚痠組、高棕櫚痠+N-乙酰半胱氨痠(N-acetyl-L-cysteine, NAC)組。各組細胞培養6、9、12 h後採用Western blotting和RT-PCR檢測各組NLRP3、Caspase-1、IL-1β蛋白及mRNA錶達,併同時觀察NAC對各組蛋白及mRNA錶達的影響。結果：棕櫚痠刺激腎繫膜細胞NLRP3炎癥小體信號分子的錶達變化：與對照組相比,不同作用濃度和時間的棕櫚痠均可上調NLRP3、Caspase-1、IL-1β蛋白及mRNA錶達(P<0.05),且呈濃度和時間依賴性。與單純棕櫚痠組相比, NAC預處理可阻止棕櫚痠誘導的NLRP3、Caspase-1、IL-1β蛋白及mRNA錶達上調(P<0.05)。結論：棕櫚痠可通過氧化應激機製誘導繫膜細胞NLRP3炎癥小體信號的活化,參與糖尿病腎病炎癥的髮生。
목적：：탐토NLRP3염증소체재유리지방산(free fatty acids, FFAs)유도하적신소구계막세포(HBZY-1)중적표체급양화응격재기중적영향。방법：장HBZY-1세포분위정상대조조、불동농도종려산조、고종려산+N-을선반광안산(N-acetyl-L-cysteine, NAC)조。각조세포배양6、9、12 h후채용Western blotting화RT-PCR검측각조NLRP3、Caspase-1、IL-1β단백급mRNA표체,병동시관찰NAC대각조단백급mRNA표체적영향。결과：종려산자격신계막세포NLRP3염증소체신호분자적표체변화：여대조조상비,불동작용농도화시간적종려산균가상조NLRP3、Caspase-1、IL-1β단백급mRNA표체(P<0.05),차정농도화시간의뢰성。여단순종려산조상비, NAC예처리가조지종려산유도적NLRP3、Caspase-1、IL-1β단백급mRNA표체상조(P<0.05)。결론：종려산가통과양화응격궤제유도계막세포NLRP3염증소체신호적활화,삼여당뇨병신병염증적발생。
Objective: To explore the expression of NLRP3 inflammasome induced by free fatty acids and the influence of oxidative stress in renal mesangial cells. Methods: Mesangial cells were randomly divided into the normal group(NC group), different concentrations of palmitic acid group(HPA group) and the NAC intervention in high palmitic group(HPA+NAC group). Each group was cultured for 6, 9 and 12 h,then detected the expressions of NLRP3, Caspase-1, IL-1β protein and mRNA by Western blotting and RT-PCR,and the influence on the protein and mRNA expression of each group induced by NAC was observed. Results: Compared with normal group, the protein and mRNA level of NLRP3, Caspase-1 and IL-1β were upregulated induced by different concentrations palmitic acid for various times,in a dose and time-dependent manner (P<0.05). Compared with palmitic acid group, the expressions of NLRP3, Caspase-1 and IL-1β were decreased after pretreatment palmitic acid growp with NAC(P< 0.05). Conclusion: Palmitic acid could induce the activation of NLRP3 inflammasome signaling in mesangial cells via reactive oxygen species and mediate inflammation in diabetic nephropathy.
