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Abstract：
Evidence suggests that sedative dexmedetomidine can prevent intestinal dysfunction. However, the specific mechanisms of its protective effects against burn-induced intestinal barrier injury remain unclear. We aimed to explore the possible positive effects of dexmedetomidine on burn-induced intestinal barrier injury and the effects the myosin light chain kinase (MLCK)/phosphorylated myosin light chain (p-MLC) signalling pathway in an experimental model of burn injury.
In this study, the plasma concentration of fluorescein isothiocyanate-labelled dextran (FITC-dextran) was measured. Histological changes were evaluated using haematoxylin and eosin (HE) staining. Tight junction proteins were evaluated by western blot and immunofluorescence analyses to assess the structural integrity of intestinal tight junctions. The level of inflammation was detected by enzyme-linked immunosorbent assay (ELISA).
The results shows that the increase in intestinal permeability caused by burn injury is accompanied by histological damage to the intestine, decreases in the expression of the tight junction proteins Zonula Occludens-1 (ZO-1) and Occludin, increases in inflammatory cytokine levels and elevation of both MLCK protein expression and MLC phosphorylation. After dexmedetomidine treatment, the burn-induced changes were ameliorated.
In conclusion, dexmedetomidine exerted an anti-inflammatory effect and protected tight junction complexes against burn‑induced intestinal barrier damage by inhibiting the MLCK/p-MLC signalling pathways.
In this study, the plasma concentration of fluorescein isothiocyanate-labelled dextran (FITC-dextran) was measured. Histological changes were evaluated using haematoxylin and eosin (HE) staining. Tight junction proteins were evaluated by western blot and immunofluorescence analyses to assess the structural integrity of intestinal tight junctions. The level of inflammation was detected by enzyme-linked immunosorbent assay (ELISA).
The results shows that the increase in intestinal permeability caused by burn injury is accompanied by histological damage to the intestine, decreases in the expression of the tight junction proteins Zonula Occludens-1 (ZO-1) and Occludin, increases in inflammatory cytokine levels and elevation of both MLCK protein expression and MLC phosphorylation. After dexmedetomidine treatment, the burn-induced changes were ameliorated.
In conclusion, dexmedetomidine exerted an anti-inflammatory effect and protected tight junction complexes against burn‑induced intestinal barrier damage by inhibiting the MLCK/p-MLC signalling pathways.
摘要：
证据表明，镇静右美托咪定可以预防肠功能障碍。然而,其对烧伤引起的肠屏障损伤的保护作用的具体机制尚不清楚.我们旨在探讨右美托咪定对烧伤诱导的肠屏障损伤的可能积极作用以及在烧伤实验模型中对肌球蛋白轻链激酶（MLCK）/磷酸化肌球蛋白轻链（p-MLC）信号通路的影响。
在这项研究中,测量异硫氰酸荧光素标记的葡聚糖(FITC-葡聚糖)的血浆浓度。使用苏木精和伊红(HE)染色评价组织学变化。通过蛋白质印迹和免疫荧光分析评估紧密连接蛋白，以评估肠紧密连接的结构完整性。采用酶联免疫吸附试验(ELISA)检测炎症水平。
结果表明，烧伤引起的肠道通透性增加伴随着对肠道的组织学损伤，紧密连接蛋白ZonulaOccludens-1（ZO-1）和Occludin的表达降低，炎性细胞因子水平的增加以及MLCK蛋白表达和MLC磷酸化的升高。右美托咪定治疗后，烧伤引起的变化得到改善。
总之,右美托咪定发挥抗炎作用,并通过抑制MLCK/p-MLC信号通路保护紧密连接复合物免受烧伤诱导的肠屏障损伤.
在这项研究中,测量异硫氰酸荧光素标记的葡聚糖(FITC-葡聚糖)的血浆浓度。使用苏木精和伊红(HE)染色评价组织学变化。通过蛋白质印迹和免疫荧光分析评估紧密连接蛋白，以评估肠紧密连接的结构完整性。采用酶联免疫吸附试验(ELISA)检测炎症水平。
结果表明，烧伤引起的肠道通透性增加伴随着对肠道的组织学损伤，紧密连接蛋白ZonulaOccludens-1（ZO-1）和Occludin的表达降低，炎性细胞因子水平的增加以及MLCK蛋白表达和MLC磷酸化的升高。右美托咪定治疗后，烧伤引起的变化得到改善。
总之,右美托咪定发挥抗炎作用,并通过抑制MLCK/p-MLC信号通路保护紧密连接复合物免受烧伤诱导的肠屏障损伤.
