英语翻译Protein expression of ET(B) and 5-HT(1B) receptors in cerebrovascular smooth muscles from SAH-induced rats was increased to 175 +/- 33.17% and 167.7 +/- 24.74%,respectively,of the levels in sham-operated rats.Endothelin-B and 5-HT(1B) exp

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英语翻译Protein expression of ET(B) and 5-HT(1B) receptors in cerebrovascular smooth muscles from SAH-induced rats was increased to 175 +/- 33.17% and 167.7 +/- 24.74%,respectively,of the levels in sham-operated rats.Endothelin-B and 5-HT(1B) exp
英语翻译
Protein expression of ET(B) and 5-HT(1B) receptors in cerebrovascular smooth muscles from SAH-induced rats was increased to 175 +/- 33.17% and 167.7 +/- 24.74%,respectively,of the levels in sham-operated rats.Endothelin-B and 5-HT(1B) expression levels in U0126-treated SAH-induced rats were at the levels in sham-operated rats (101.9 +/- 13.38% and 91.44 +/- 16.75%,respectively).In a rotating pole test used to assess gross sensorimotor function on the 2nd day after surgery,sham-operated rats achieved an average score of 5.37 +/- 0.23,SAH-induced rats scored 3.35 +/- 0.67,and SAH-induced U0126-treated rats scored 5.00 +/- 0.4.CONCLUSIONS:The authors demonstrated that experimental SAH induces upregulation of ET(B) and 5-HT(1B) receptors in cerebrovascular smooth muscles and that treatment with the MEK1/2 inhibitor U0126 abolishes this receptor upregulation.They also demonstrated that experimental SAH results in sensorimotor deficits as assessed by a rotating pole test.These deficits were alleviated by U0126 treatment,suggesting that cerebrovascular receptor upregulation is critical for the functional outcome of delayed cerebral ischemia.The authors suggest that inhibition of MEK1/2 may be a promising new SAH treatment strategy.

英语翻译Protein expression of ET(B) and 5-HT(1B) receptors in cerebrovascular smooth muscles from SAH-induced rats was increased to 175 +/- 33.17% and 167.7 +/- 24.74%,respectively,of the levels in sham-operated rats.Endothelin-B and 5-HT(1B) exp
ET（乙）和5 - 羟色胺（1B）从蛛网膜下腔出血引起的大鼠脑血管平滑肌受体蛋白表达增加至175+/ - 33.17％和167.7+/ - 24.74％,分别为水平,假手术大鼠.在U0126处理后蛛网膜下腔出血引起的大鼠内皮素-B和5 - 羟色胺（1B）的表达水平,假手术组大鼠的水平（101.9+/ - 13.38％和91.44+/ - 16.75％,分别）.在旋转杆,用来评估在手术后第2天,总感觉功能测试,假手术组大鼠的平均得分达到5.37+/ - 0.23,蛛网膜下腔出血引起的大鼠拿下3.35+/ - 0.67,和蛛网膜下腔出血引起的U0126处理治疗组5.00+ / - 0.4分.结论：作者表明,实验性SAH诱导上调ET（乙）和5 - 羟色胺（1B）受体在脑血管平滑肌和MEK1/ 2抑制剂U0126废除这种受体上调的治疗.他们还感觉赤字蛛网膜下腔出血,实验结果证明,由一个旋转杆测试评估.U0126可处理这些赤字得到缓解,这表明脑受体上调为迟发性脑缺血的功能的结果是至关重要的.作者认为,抑制MEK1 / 2的可能是一个充满希望的新的蛛网膜下腔出血的治疗策略.

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蛋白表达内皮素（乙）和5 - HT（B）受体在脑血管平滑肌从蛛网膜下腔出血后大鼠增加175 + / - 33.17%和167.7 + / - 24.74%的水平，分别为，在假手术大鼠。内皮素B和5 -羟色胺（1）的表达水平在u0126-treated蛛网膜下腔出血后大鼠在水平的假手术大鼠（101.9+ / -13.38%和91.44 + / -16.75%，分别）。在旋转杆测试用于评估感觉运动功能在手术后第二天，假手术大鼠的平均得分为5.37 + / - 0.23，蛛网膜下腔出血后大鼠的得分3.35 + / -0.67，和蛛网膜下腔出血后大鼠u0126-treated得分5 + / -0.4。结论：作者的实验表明，蛛网膜下腔出血诱导上调内皮素（乙）和5 - HT（B）受体在脑血管平滑肌和治疗与MEK 1/2抑制剂U 0126废除这一受体上调。他们还表明，实验性蛛网膜下腔出血的结果感觉赤字评估由一个旋转杆试验。这些赤字缓解U 0126处理，这表明脑受体上调是至关重要的功能结果迟发性脑缺血。作者建议，抑制MEK 1/ 2可能是一个充满希望的新的蛛网膜下腔出血的治疗策略。

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蛋白的表达等(B)和5 -羟色胺(1 B)受体在脑血管平滑肌从SAH-induced老鼠增加到175 + / - 33.17%和167.7 + / - 24.74%,分别在sham-operated老鼠的水平。Endothelin-B和5 -羟色胺(1 B)表达水平在U0126-treated SAH-induced老鼠的水平,在sham-operated老鼠(101.9 + / - 13.38%和91.44 + / - 16.75%)。在一个旋转杆测试用来评估总感觉运动功能在手术后第二天,sham-operated老鼠达到平均分数为5.37 + / - 0.23,SAH-induced老鼠得分3.35 + / - 0.67,和SAH-induced U0126-treated老鼠得分5.00 + / - 0.4。结论:作者证明实验SAH归纳的upregulation ET(B)和5 -羟色胺(1 B)受体在脑血管平滑肌和治疗与MEK1/2抑制剂U0126废除这个受体upregulation。他们也证明了实验SAH导致感觉运动赤字作为评估一个旋转杆测试。这些赤字是由U0126治疗缓解,这表明脑血管受体upregulation来说非常关键功能结果脑缺血的延迟。作者建议,抑制MEK1/2可能是一个有前途的新长官的治疗策略。

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