间充质干细胞抑制MEK/ERK信号通路改善盲肠结扎穿孔所致急性肺损伤中肺泡Ⅱ型上皮细胞的凋亡

摘 要: 【目的】 研究间充质干细胞(MSC)可通过抑制MEK/ERK信号通路改善脓毒症所致急性肺损伤(ALI)中肺泡Ⅱ型上皮细胞(AECⅡ)凋亡水平? 【方法】 本研究取30只balb/c雄性小鼠,随机抽取其中20只通过盲肠结扎穿孔(CLP)建立小鼠脓毒症所致急性肺损伤的模型,CLP术后6h随机分成2组,每组10只,通过尾静脉分别注射间充质干细胞(MSC)?生理盐水,同时将剩余10只小鼠建立假手术组作为对照组?该三组分别命名为CLP/MSC?CLP/saline?SHAM?CLP术后24 h收集肺组织及肺泡灌洗液(BALF)进行模型评估及分析检测?通过与抗生素联用,分析3组7 d生存率差异?...

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Published inZhongshan da xue xue bao. Zhongshan daxue xuebao yixue kexue ban = Journal of Sun Yat-sen University. Yi xue ke xue ban Vol. 37
Format Journal Article
LanguageChinese
Published Editorial Office of Journal of Sun Yat-sen University 01.01.2016
Subjects
凋亡
急性肺损伤/急性呼吸窘迫综合症
细胞外信号调节激酶
脓毒症
间充质干细胞
Online AccessGet full text
ISSN1672-3554

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Abstract 摘 要: 【目的】 研究间充质干细胞(MSC)可通过抑制MEK/ERK信号通路改善脓毒症所致急性肺损伤(ALI)中肺泡Ⅱ型上皮细胞(AECⅡ)凋亡水平? 【方法】 本研究取30只balb/c雄性小鼠,随机抽取其中20只通过盲肠结扎穿孔(CLP)建立小鼠脓毒症所致急性肺损伤的模型,CLP术后6h随机分成2组,每组10只,通过尾静脉分别注射间充质干细胞(MSC)?生理盐水,同时将剩余10只小鼠建立假手术组作为对照组?该三组分别命名为CLP/MSC?CLP/saline?SHAM?CLP术后24 h收集肺组织及肺泡灌洗液(BALF)进行模型评估及分析检测?通过与抗生素联用,分析3组7 d生存率差异?【结果】 模型制备达到ALI水平?在肺损伤程度上,经MSC治疗后,髓过氧化物酶(MPO)活性?肺血管通透性及病理表现,经MSC治疗后较CLP/saline组均有明显改善?7 d生存率CLP/MSC?CLP/saline分别为32%和0(P < 0.05),CLP术后24 h BALF中SP-A含量 CLP/MSC组(3115 ± 93)ng/mL较CLP/saline组(2344 ± 192)ng/mL明显改善(P = 0.002)?CLP/MSC组AECⅡ凋亡水平较CLP/saline组明显降低(P = 0.001)?肺组织fas?bax/bcl-2及caspase3 mRNA扩增倍数CLP/Saline vs CLP/MSC p值分别为0.09?0.004及0.037,均 < 0.05,蛋白水平fas?bax/bcl-2?cleaved caspase3?p-MEK?p-ERK CLP/MSC组较CLP/saline组也明显降低?结论 MSC可能是通过抑制MEK/ERK信号通路磷酸化,影响外源性死亡受体(FAS/FASL)途径及内源性(线粒体)凋亡途径来减少ALI中肺泡上皮细胞尤其是AECⅡ凋亡,从而在一定程度上降低ALI死亡率?
AbstractList 摘 要: 【目的】 研究间充质干细胞(MSC)可通过抑制MEK/ERK信号通路改善脓毒症所致急性肺损伤(ALI)中肺泡Ⅱ型上皮细胞(AECⅡ)凋亡水平? 【方法】 本研究取30只balb/c雄性小鼠,随机抽取其中20只通过盲肠结扎穿孔(CLP)建立小鼠脓毒症所致急性肺损伤的模型,CLP术后6h随机分成2组,每组10只,通过尾静脉分别注射间充质干细胞(MSC)?生理盐水,同时将剩余10只小鼠建立假手术组作为对照组?该三组分别命名为CLP/MSC?CLP/saline?SHAM?CLP术后24 h收集肺组织及肺泡灌洗液(BALF)进行模型评估及分析检测?通过与抗生素联用,分析3组7 d生存率差异?【结果】 模型制备达到ALI水平?在肺损伤程度上,经MSC治疗后,髓过氧化物酶(MPO)活性?肺血管通透性及病理表现,经MSC治疗后较CLP/saline组均有明显改善?7 d生存率CLP/MSC?CLP/saline分别为32%和0(P < 0.05),CLP术后24 h BALF中SP-A含量 CLP/MSC组(3115 ± 93)ng/mL较CLP/saline组(2344 ± 192)ng/mL明显改善(P = 0.002)?CLP/MSC组AECⅡ凋亡水平较CLP/saline组明显降低(P = 0.001)?肺组织fas?bax/bcl-2及caspase3 mRNA扩增倍数CLP/Saline vs CLP/MSC p值分别为0.09?0.004及0.037,均 < 0.05,蛋白水平fas?bax/bcl-2?cleaved caspase3?p-MEK?p-ERK CLP/MSC组较CLP/saline组也明显降低?结论 MSC可能是通过抑制MEK/ERK信号通路磷酸化,影响外源性死亡受体(FAS/FASL)途径及内源性(线粒体)凋亡途径来减少ALI中肺泡上皮细胞尤其是AECⅡ凋亡,从而在一定程度上降低ALI死亡率?
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PublicationTitle Zhongshan da xue xue bao. Zhongshan daxue xuebao yixue kexue ban = Journal of Sun Yat-sen University. Yi xue ke xue ban
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Snippet 摘 要: 【目的】 研究间充质干细胞(MSC)可通过抑制MEK/ERK信号通路改善脓毒症所致急性肺损伤(ALI)中肺泡Ⅱ型上皮细胞(AECⅡ)凋亡水平? 【方法】...
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SubjectTerms 凋亡
急性肺损伤/急性呼吸窘迫综合症
细胞外信号调节激酶
脓毒症
间充质干细胞
Title 间充质干细胞抑制MEK/ERK信号通路改善盲肠结扎穿孔所致急性肺损伤中肺泡Ⅱ型上皮细胞的凋亡
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Volume 37
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