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首页> 外文期刊>Cellular and molecular biology >GSK2193874 treatment at heatstroke onset reduced cell apoptosis in heatstroke mice
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GSK2193874 treatment at heatstroke onset reduced cell apoptosis in heatstroke mice

机译:热量小鼠中暑的GSK2193874治疗减少细胞凋亡

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摘要

Heatstroke is still a potentially fatal threat during summer heat waves, despite improved prevention and treatment. It is reported that the transient receptor potential vanilloid 4 (TRPV4) inhibitoi may protect septicemia mice. Many aspects ot heatstroke have been defined, from the sepsis-mimic inflammatory response to hxperthermia Hence, TRPV4 may be a therapeutic target for heatstroke. The results in murine models of heatstroke verified that GSK2193874 as a selected TRPV4 inhibitor, was injected at heatstroke onset, and then reduced the reduction of core temperature the death rate, wet/dry ratio of the lung, levels of tumor necrosis factor-alpha (TNTF-alpha) and mterleukin (IL)-6, coagulation indicators, the degree of organ injury, and caspase-3/7 activity (P 0.05). But GSK2193874 treatment before heat stress did not improve the svmptoms of heatstroke mice. Therefore TRPV4 should be involved in heatstroke-induced injury. Timely GSK2193874 admmistiation may be useiul to reduce heatstroke-induced injury. TRPV4 may be a potential new therapeutic target in fatal heatstroke.
机译:尽管改善了预防和治疗,但热量在夏季热浪期间仍然是一个可能的致命威胁。据报道,瞬时受体潜在的香草4(TRPV4)抑制剂可以保护败血症小鼠。许多方面已经定义了OT热量,从败血症 - 模拟炎症反应对肾病热,因此,TRPV4可以是用于中暑的治疗靶标。鼠中热线口鼠模型的结果验证了GSK2193874作为选定的TRPV4抑制剂,在中暑上注射,然后减少了核心温度的降低,肺部的肺率,湿润/干比,肿瘤坏死因子-α的水平( TNTF-α)和MTerleukin(IL)-6,凝血指示剂,器官损伤程度和Caspase-3/7活性(P <0.05)。但GSK2193874在热应激之前的处理未改善中暑小鼠的SVMPTOM。因此,TRPV4应参与中暑诱导的损伤。及时GSK2193874展会可能是用途减少中暑诱导的损伤。 TRPV4可以是致命中暑的潜在的新治疗靶标。

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