CAJ | 학술논문

目的观察不同剂量盐酸戊乙奎醚(penehyclidine hydrochloride,PHC)对创伤性休克后大鼠肺组织NF - κB和诱导型一氧化氮合酶(inducible nitric oxide synthase.iNOS) mRNA表达的干预影响,探讨PHC对创伤性休克继发肺损伤的作用及可能机制.方法建立创伤性休克动物模型,104只Wistar大鼠按随机数字表法分成四组:对照组、休克组、PHC小剂量组(P1组)和PHC大剂量组(P2组).复苏开始时,P1、P2组大鼠分别经颈静脉注入含PHC 0.15 mg/kg和0.45 mg/kg的等渗盐水,给药容积2 ml/kg；休克组、对照组仅注入等容积的等渗盐水.复苏后2,6,12,24 h四个时相点处死大鼠.RT - PCR法检测各组NF - κB、iNOS mRNA表达；计算肺湿/干重(W/D)比值、肺通透指数(lung permeability index,LPI)和肺损伤评分(lung injury score,LIS).结果与对照组比较,休克组、P1、P2组各时相点NF - κB、iNOS mRNA表达、肺W/D比值、LPI、LIS均明显增高( P＜0.05).与休克组比较,P2组复苏后各时相点及P1组复苏后2,6 h NF- κB、iNOS mRNA表达、肺W/D比值、LPI、LIS明显减低,同时P1组复苏后12 h LPI、LIS也明显降低.P2组6 h NF- κB、iNOS mRNA表达、肺W/D比值、LPl、LIS均明显低于P1组(P＜0.05).结论 PHC可减轻创伤性休克后继发肺损伤,大剂量PHC作用更强,其机制可能与抑制肺组织NF - κB、iNOS mRNA表达有关.
목적 관찰불동제량염산무을규미(penehyclidine hydrochloride,PHC)대창상성휴극후대서폐조직NF - κB화유도형일양화담합매(inducible nitric oxide synthase.iNOS) mRNA표체적간예영향,탐토PHC대창상성휴극계발폐손상적작용급가능궤제.방법 건립창상성휴극동물모형,104지Wistar대서안수궤수자표법분성사조:대조조、휴극조、PHC소제량조(P1조)화PHC대제량조(P2조).복소개시시,P1、P2조대서분별경경정맥주입함PHC 0.15 mg/kg화0.45 mg/kg적등삼염수,급약용적2 ml/kg；휴극조、대조조부주입등용적적등삼염수.복소후2,6,12,24 h사개시상점처사대서.RT - PCR법검측각조NF - κB、iNOS mRNA표체；계산폐습/간중(W/D)비치、폐통투지수(lung permeability index,LPI)화폐손상평분(lung injury score,LIS).결과 여대조조비교,휴극조、P1、P2조각시상점NF - κB、iNOS mRNA표체、폐W/D비치、LPI、LIS균명현증고( P＜0.05).여휴극조비교,P2조복소후각시상점급P1조복소후2,6 h NF- κB、iNOS mRNA표체、폐W/D비치、LPI、LIS명현감저,동시P1조복소후12 h LPI、LIS야명현강저.P2조6 h NF- κB、iNOS mRNA표체、폐W/D비치、LPl、LIS균명현저우P1조(P＜0.05).결론 PHC가감경창상성휴극후계발폐손상,대제량PHC작용경강,기궤제가능여억제폐조직NF - κB、iNOS mRNA표체유관.
Objective To observe the interfering effect of different doses of penehyclidine hydrochloride (PHC) on the mRNA expressions of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the lung tissue of rats with traumatic shock so as to investigate the protective role of PHC in secondary long injury following traumatic shock and the underlying mechanism.Methods The traumatic shock model was established.A total of 104 Wistar rats were randomly divided into four groups:control group,shock group,low dose PHC group ( P1 group) and high dose PHC group ( P2 group).At the beginning of resuscitation,the rats in P1 and P2 groups were given transjugular intravenous injection of 2 ml/kg isotonic saline containing 0.15 mg/kg and 0- 45 mg/kg PHC respectively,while the rats in shock and control groups were injected only isometric isotonic saline.The rats in the four groups were killed at 2 h,6 h,12 h and 24 h after resuscitation respectively to detect the mRNA expressions of NF-κB and iNOS by using RT-PCR and determine the lung wet/dry weight (W/D) ratio,lung permeability index (LPI) and lung injury score (LIS).Results The mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS at all the time intervals in the shock,P1 and P2 groups were all significantly increased as compared with those in the control group (P＜0.05).Howerver,the P2 group showed significant reduction in aspects of the mRNA expressions of NF- κB and iNOS,lung W/D ratio,LPI and LIS at all time points and P1 group also had significant decrease regarding the mRNA expressions of NF-κB and iNOS,lung W/D ratio at2 h,6 h,and LPI and LIS at 2 h,6 h,12 h,as compared with the shock group.Meanwhile,P2 group showed evident decrease at 6 h concerning the mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS as compared with P1 group (P ＜ 0.05 ).Conclusions PHC,especially at a large dosage,can significantly mitigate the long injury secondary to traumatic shock,and the mechanism may be associated with the inhibition of mRNA expressions of NF-κB and iNOS.