中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2015年
9期
1185-1188,1189
,共5页
邓雪红%邢小燕%李光%张美双%石金金%孙桂波%孙晓波
鄧雪紅%邢小燕%李光%張美雙%石金金%孫桂波%孫曉波
산설홍%형소연%리광%장미쌍%석금금%손계파%손효파
缺血/再灌注损伤%辅助性T细胞%Th1/Th2%免疫反应%中药%多靶点
缺血/再灌註損傷%輔助性T細胞%Th1/Th2%免疫反應%中藥%多靶點
결혈/재관주손상%보조성T세포%Th1/Th2%면역반응%중약%다파점
ischemia-reperfusion injury%helper T cell%Th1 /Th2%immune response%traditional Chinese medicine%multi-target
缺血组织恢复血流后,组织损伤程度急剧增加,免疫反应是缺血/再灌注造成组织二次损伤的关键因素之一。Th1/Th2在正常机体中处于免疫平衡状态,在缺血/再灌注环境下,易发生 Th1/Th2漂移,形成 Th1优势状态,介导细胞免疫。过度的免疫反应即可引起细胞凋亡和组织损伤。研究发现,诱导 Th1优势状态向 Th2优势状态转化,是治疗缺血/再灌注损伤的可行途径。随着多组分、多靶点的现代药物研发模式的兴起,中药在治疗复杂疾病中的优势凸显。该文从Th1/Th2失衡与缺血/再灌注损伤关系及中药在该疾病中的应用前景进行了综述。
缺血組織恢複血流後,組織損傷程度急劇增加,免疫反應是缺血/再灌註造成組織二次損傷的關鍵因素之一。Th1/Th2在正常機體中處于免疫平衡狀態,在缺血/再灌註環境下,易髮生 Th1/Th2漂移,形成 Th1優勢狀態,介導細胞免疫。過度的免疫反應即可引起細胞凋亡和組織損傷。研究髮現,誘導 Th1優勢狀態嚮 Th2優勢狀態轉化,是治療缺血/再灌註損傷的可行途徑。隨著多組分、多靶點的現代藥物研髮模式的興起,中藥在治療複雜疾病中的優勢凸顯。該文從Th1/Th2失衡與缺血/再灌註損傷關繫及中藥在該疾病中的應用前景進行瞭綜述。
결혈조직회복혈류후,조직손상정도급극증가,면역반응시결혈/재관주조성조직이차손상적관건인소지일。Th1/Th2재정상궤체중처우면역평형상태,재결혈/재관주배경하,역발생 Th1/Th2표이,형성 Th1우세상태,개도세포면역。과도적면역반응즉가인기세포조망화조직손상。연구발현,유도 Th1우세상태향 Th2우세상태전화,시치료결혈/재관주손상적가행도경。수착다조분、다파점적현대약물연발모식적흥기,중약재치료복잡질병중적우세철현。해문종Th1/Th2실형여결혈/재관주손상관계급중약재해질병중적응용전경진행료종술。
The damage of tissue increases dramatically after reperfusion of blood supply to ischemic tissues.Immune response is one of the key reasons of ischemia-reperfusion injury.Th1 /Th2 generally stays balanced in normal states.Under the envi-ronment of ischemia reperfusion,Th1 /Th2 shifting let Th1 domi-nant to mediate cellular immunity.Excessive immune reaction may cause cell apoptosis and tissue damage.Recent studies showed that induction of transferring Th1 dominant to Th2 domi-nant was feasible for the treatment of ischemia-reperfusion inju-ry.With the progress of modern drug development paradigm“multi-composition,multi-target”,Chinese medicine has advan-tages in treating complex diseases.This paper summarizes the research of the relationship between Th1 /Th2 imbalance and is-chemia-reperfusion injury,together with the prospects of tradi-tional Chinese medicine with multi-target effect in ischemia-reperfusion injury.