Influence Of Inflammatory Cytokines Produce In Human Pregnant Myometrial By CRH

Premature birth remains a major cause of infant morbidity and is a serious healthand financial burden to society. And premature mortality about15%. Because theetiology for premature labor is not clear, the incidence of premature birth has not beeneffective control.In normal circumstances, pregnancy before the term, the uterus is in a relativelyresting state, its low excitability. The pre-excitement of uterine smooth muscle willlead to preterm labor. While in human the events that trigger parturition are not welldefined, prior to the onset of parturition. The present study showed that the fetus frommaternal and many factors in the interaction between the uterine muscle by restingstate into contraction condition. These factors include known steroid hormone, promoteadrenal hormone release hormones, inflammatory mediators, prostaglandins, and manywith paracrine/autocrine way effects of molecules. But it is not clear exactly how thesefactors work.Placental CRH production increases exponentially as pregnancy progressestoward labor, and it has been proposed that CRH might act as a placental clockregulating the length of human gestation. Human uterine muscle can express CRHreceptors, suggests human uterine muscle is CRH role of target organs. In recent years,studies show that uterine activate delivery is an inflammatory reaction process. Late inpregnancy, a number of leukocyte infilter myometrium and cervical, myometrium alsoshows a significant inflammation response state, a lot of leukocyte infiltration, swellingand some inflammatory cytokines and the expression of the markers, and so on.In my study,used of RT-polymerase chain reaction (PCR) observe the changesand inflammatory cytokines mRNA radiation immune method for determining the cellsof the liquid protein content of the qing dynasty, the CRH before and after birth ofmyometrium cell inflammatory cytokines influence of produce.Main results and conclusions are as follows:Influence of Inflammatory Cytokines Produce in Human PregnantMyometrial by CRH1) For the labouring myometrium,CRH did not induce inflammatorycytokines in myometium cells. The effects,CRH increase the inflammatorycytokines（IL-6、IL-8、MCP-1） in myometrium from nonlaboring.2) We used CRHR small interfering RNA (siRNA) abrogate the effect of inflammatory cytokines increase in nonlaboring myometrium cell stimulated byCRH,were reversed by CRH receptor type1(CRHR1) antagonist antalarmin. Theeffects of antalarmin could be blocked by exogenous CRH, suggesting thatendogenous CRH has tonic inhibitory effects on inflammatory cytokines.3) We used CRHR2small interfering RNA (siRNA) abrogate the effect ofinflammatory cytokines increase in nonlaboring myometrium cell stimulated byCRH. Treatment of myometrium cells with AC agonist Forskolin caused a increasein the protein expression as well as CRH and inhibitor SQ caused a decrease in theprotein produce.4) We used CRHR2small interfering RNA (siRNA) abrogate the effect ofinflammatory cytokines increase in nonlaboring myometrium cell stimulated byCRH. The effects,CRH increase the level of the cAMP in myometrium;treatmentof myometrium cells with CRH antagonist antalarmin caused a decrease in theprotein expression as well as the CRH.5) We used CRHR2small interfering RNA (siRNA) abrogate the effect ofinflammatory cytokines increase in nonlaboring myometrium cell stimulated byCRH. Treatment of myometrium cells with the inhibitor H89of PKA caused adecrease in the protein expression as well as CRH.6) We used CRHR2small interfering RNA (siRNA) abrogate the effect ofinflammatory cytokines increase in nonlaboring myometrium cell stimulated byCRH. Alone treated with the inhibitor of NF-kB decrease in the protein expressionas well as CRH.But treatment of myometrium cells with the inhibitor of NF-kB andForskolin not induce in the protein expression as well as CRH.In summary, the above results demonstrated:Our the results showed that there is a correlation between the inflammatorycytokines and CRH.The results suggest that CRH act on CRHR1to increaseinflammatory cytokines in nonlabouring myometrium. Before labour onset, CRHR1may stimulates AC-cAMP-PKA signaling pathway to increase inflammatory cytokinesmyometrium cells. Also, the nuclear factor kappa-B(NF-кB)would be stimulated in thissignalings. Thus, the present study indicates that CRH may modulate the humaninflammatory cytokines function in nonlabouring myometrium by AC-cAMP-PKAsignaling pathway and NF-кB.