摘要
目的初步探讨PKCγ、PKCβⅡ在内脏炎症痛过程中的作用。方法本实验用福尔马林复制的内脏炎症痛模型,经脊髓蛛网膜下腔插管给予PKCγ、PKCβⅡ激动剂PMA(phorbol 12-myristate 13-acetate)和抑制剂H-7(1-(5-isoquinolinesulfonyl)2-methylpiperazine dihydrochloride),结合SDS-聚丙烯酰胺凝胶电泳(SDS-PAGE)、蛋白印迹(Western-blot)等生化技术,选用成年健康Wistar大鼠,随机分4组:N;F+IT+NaCl;F+IT+PMA;F+IT+H-7。共分福尔马林直肠内致炎后30 min6、0 min和120 min三个时间段。结果在福尔马林直肠致炎后30 min内,F+IT+NaCl组与N组PKCγ膜转位相比明显增多(P<0.01),F+IT+PMA组与F+IT+Na-Cl组相比明显减少(P<0.05),F+IT+H-7组与F+IT+NaCl组相比明显增高(P<0.05);在福尔马林直肠致炎后的30 min6、0 min和120 min三个时间段内,PKCβII膜转位没有明显变化(P>0.05)。结论福尔马林致内脏炎症痛过程中PKCγ被激活,PKCβII没有被激活,提示PKCγ可能参与了内脏炎症痛的发生;PKCβII可能没有参与内脏炎症痛的发生。
Obiective： To explore the role of PKCγ and PKCβⅡ in visceral inflammatory pain. Methods： A model of visceral inflammatory pain induced by formalin and the biochemistry techniques of SDS-PAGE and Western bolt were used to examine the changes of PKCγ and PKCPKCβⅡ membrane translocation by intrathecal injection of PMA（ phorbol 12- myristate 13 - acetate） and H 7 （ 1 - （5 - isoquinolinesulfonyl） 2-methylpiperazine dihydrochroride）, which are activator and inhibitor of PKCγ and PKCβⅡ respectively . Adult healthy Wistar rats were used and divided into 4 groups random- ly： group N; group F ＋ IT ＋ NaCl; group F ＋ IT ＋ PMA and F ＋ IT ＋ H - 7. There are three time points： 30min, 60min and 120min. Resalts： Significant changes in membrane translocation of PKCγ were ,seen in the former 30min between group F ＋ IT ＋ NaCl and group N （P 〈 0.01 ） ; between group F ＋ IT ＋ PMA and F ＋ IT ＋ NaCl （ P 〈 0.05 ） ; between group F ＋ IT ＋ H - 7 and F ＋ IT ＋ NaCl （ P 〈; 0.05 ）. No significance of membrane translocation of PKCβⅡ was shown in three time points （P ;〉 0.05）. Conclusion： PKCγis activated in visceral inflammatory pain induced by formalin; while PKCβⅡ is not. It indicates that PKCγ involves in the progress of visceral inflammatory pain; while PKCβⅡprobably does not.
出处
《泰山医学院学报》
CAS
2005年第4期284-287,共4页
Journal of Taishan Medical College
关键词
大鼠
福尔马林
蛋白激酶C
膜转位
内脏
疼痛
rat
formalin
protein kinase C
membrane translocation
visceral pain
