Tang Jia, Guo Chunbao, Gong Fang
Department of Pediatrics, Yongchuan Hospital Affiliated to Chongqing Medical University, Chongqing 402160, China.
Department of Hepatobiliary Surgery, Children's Hospital Affiliated to Chongqing Medical University, Chongqing 400016, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2019 Oct 30;39(10):1221-1226. doi: 10.12122/j.issn.1673-4254.2019.10.14.
To investigate the protective effect of DSM17938 strain against oxidative stress in a neonatal mouse model of necrotizing enterocolitis (NEC) and explore the possible mechanism.
Ninety-six 10-day-old neonatal C57BL/6J mice were equally randomized into control group, NEC group, and NEC+ group. The pathological changes of the ileocecal intestinal tissue were evaluated with HE staining and double-blind pathological scoring. The mRNA and protein expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the intestinal tissues were detected using quantitative real-time PCR and ELISA, respectively. Colorimetric assays were used to determine the activity of superoxide dismutase (SOD) and its inhibition rate, malondialdehyde (MDA), glutathione (GSH), oxidized glutathione (GSSG), and GSSG/ GSH ratio.
Compared with those in the control group, the neonatal mice in NEC group showed significant weight loss ( < 0.05), obvious intestinal injury, increased pathological scores ( < 0.05), increased expressions of TNF-α and IL-1β mRNA and proteins ( < 0.05), decreased SOD activity and inhibition rate, decreased GSH, and significantly increased MDA, GSSG, and GSSG/GSH ratios ( < 0.05). Treatment with obviously decreased the pathological scores, expressions of TNF-α and IL-1β ( < 0.05), MDA, GSSG, and GSSG/GSH ratio ( < 0.05), and significantly increased SOD activity, its inhibition rate, and GSH level in the mice with NEC, but the survival rate was not significantly different between NEC and -treated groups ( > 0.05).
DSM17938 can offer protection against NEC in mice by reducing oxidative stress and increasing antioxidant capacity of the intestinal tissue to suppress intestinal inflammations.
在坏死性小肠结肠炎(NEC)新生小鼠模型中研究DSM17938菌株对氧化应激的保护作用,并探讨其可能机制。
将96只10日龄新生C57BL/6J小鼠平均随机分为对照组、NEC组和NEC+组。采用HE染色和双盲病理评分评估回盲部肠组织的病理变化。分别用定量实时PCR和ELISA检测肠组织中肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的mRNA和蛋白表达。采用比色法测定超氧化物歧化酶(SOD)活性及其抑制率、丙二醛(MDA)、谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)以及GSSG/GSH比值。
与对照组相比,NEC组新生小鼠体重显著下降(<0.05),肠损伤明显,病理评分增加(<0.05),TNF-α和IL-1β mRNA及蛋白表达增加(<0.05),SOD活性和抑制率降低,GSH减少以及MDA、GSSG和GSSG/GSH比值显著增加(<0.05)。DSM17938治疗明显降低了NEC小鼠的病理评分、TNF-α和IL-1β表达(<0.05)、MDA、GSSG和GSSG/GSH比值(<0.05),并显著提高了SOD活性、其抑制率和GSH水平,但NEC组和DSM17938治疗组之间的存活率无显著差异(>0.05)。
DSM17938可通过减轻氧化应激和提高肠组织抗氧化能力以抑制肠道炎症,从而对小鼠NEC起到保护作用。