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核桃油对葡聚糖硫酸钠诱导小鼠结肠炎的影响 |
Effect of walnut oil on dextran sulfate sodium induced colitis in mice |
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DOI: |
中文关键词: 核桃油 葡聚糖硫酸钠 结肠炎 Nod样受体蛋白-3 炎性因子 保护作用 |
英文关键词:walnut oil dextran sulfate sodium (DSS) colitis Nod-like receptor pyrin domain 3 (NLRP3) inflammatory factor protective effect |
基金项目:云南省重大科技专项(2018ZG003) |
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中文摘要: |
探讨核桃油(WO)对葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的保护作用。将昆明种小鼠随机分为4组,即正常对照组(Con)、DSS组、DSS+WO组和WO组,检测小鼠血清促炎因子、结肠组织抗氧化酶活性和Nod样受体蛋白-3(NLRP3)及相关mRNA的转录水平。结果表明:与Con组相比,DSS组小鼠血清白细胞介素1β(IL-1β)和IL-6含量,结肠NLRP3、半胱氨酸蛋白酶-1(Caspase-1)和IL-1β mRNA转录水平及NLRP3蛋白表达水平极显著增高(p<0.01),结肠超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活性极显著下降(p<001);与DSS组相比,DSS+WO组血清IL-1β和IL-6含量、结肠NLRP3和Caspase-1 mRNA转录水平及NLRP3蛋白表达水平极显著降低(p<0.01),结肠SOD、GSH-Px和CAT活性极显著增强(p<001)。核桃油通过增强结肠的抗氧化能力,并可能通过抑制NLRP3炎性小体通路基因的转录水平,降低相关炎性因子的表达水平,对DSS诱导的小鼠结肠炎发挥保护作用。 |
英文摘要: |
The protective effect of walnut oil (WO) on dextran sulfate sodium (DSS) induced colitis in mice was investigated. Kunming mice were randomly divided into four groups: control group (Con), DSS group, DSS+WO group and WO group. Serum proinflammatory factors, antioxidant enzyme activity in colon tissue, Nod-like receptor pyrin domain 3 (NLRP3) and related mRNA levels were detected. The results showed that, compared with Con group, the contents of serum IL-1β and IL-6, transcription levels of NLRP3, Caspase-1 and IL-1β mRNA and NLRP3 protein expression level in colon of DSS group significantly increased (p<0.01), and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in colon significantly decreased (p<0.01). Compared with DSS group, the contents of serum IL-1β and IL-6, transcription levels of NLRP3 and Caspase-1 mRNA and NLRP3 protein expression level in colon of DSS+WO group significantly decreased (p<001), and the activities of SOD, GSH-Px and CAT in colon significantly increased (p<0.01). Walnut oil might play a protective role in DSS induced colitis in mice by enhancing the antioxidant capacity of the colon and possibly reducing the expression level of related inflammatory factors by inhibiting the transcription level of NLRP3 inflammasome pathway genes. |
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