本试验通过检测大鼠肠道中热休克蛋白基因的表达,探究不同剂量香苇二石口服液对热应激的预防和治疗作用。45只健康雄性大鼠随机分为对照组、热应激组、自然恢复组、高剂量预防组、中剂量预防组、低剂量预防组、高剂量治疗组、中剂量治疗组、低剂量治疗组,建立高温应激模型,利用Real time-PCR技术检测大鼠小肠中HSP27、HSP70、HSP90 m RNA的表达变化。结果表明,高温刺激能极显著增加HSPs m RNA的表达量(P<0.01);香苇二石口服液能显著(P<0.05)和极显著(P<0.01)抑制HSPs m RNA的高表达。表明香苇二石口服液高剂量有极显著预防作用,中剂量有极显著治疗作用。
Objective： Heat stress （HS） is an important environmental stressor that adversely influences livestock during the summer. The aim of this study was to investigate whether magnolol protects against HS-induced intestinal epithelial cell injury. Materials and methods： An intestinal epithelial cell line （IEC-6） was subjected to HS at 42℃, with and without magnolol pretreatment. Cell injury was detected by monitoring lactate dehydrogenase （LDH） release. MTS （3-（4,5-dimethyithiazol-2-yl）-5-（3-carboxymethoxyphenyl）-2-（4-sulfophenyl）-2H-tetrazolium） assay was used to as- sess cell proliferation and viability, including identifying effective concentrations of magnolol. Flow cytometry confirmed Gl-phase cell-cycle arrest and its alleviation by magnolol. Active DNA synthesis was measured by incorporation of nucleic acid 5-ethynyl-2＇-deoxyuridine （EdU）. Gl-phase cell-cycle-related gene expression was assessed by real-time reverse transcription polymerase chain reaction （RT-PCR） and levels of Gl-phase-related proteins by Western blotting Results： HS induced IEC-6 cell injury and decreased cell viability, as demonstrated by data from LDH and MTS assays respectively. Based on a number of criteria, IEC-6 cells subjected to HS were arrested in the G1 phase Of the cell cycle. Magnolol pretreatment decreased HS-induced cell injury through relief of this cell-cycle arrest. Conclusions： Magnolol pretreatment attenuates HS-induced injury in IEC-6 cells. Magnolol is potentially promising as a protective strategy for HS in livestock.
