摘要
目的:研究低O2高CO2性肺动脉高压时大鼠肺组织内硫化氢体系的变化及川芎嗪对其的干预作用。方法:将30只SD大鼠随机分为3组,每组10只。正常对照组(C组)、低O2高CO2组(HH组)、低O2高CO2+川芎嗪组(HH+LTZ组)。监测其血流动力学变化,光镜观察肺细小动脉管壁面积/管总面积比值(WA/TA),检测右心室/左心室+室间隔(RV/LV+SP)比值,原位缺口末端标记法(TUNEL法)观测肺细小动脉凋亡情况,并计算凋亡指数。敏感硫电极法测定血浆H2S含量及肺组织匀浆胱硫醚-γ-裂解酶(CSE)活性变化。RT-PCR法测定肺组织中CSE基因表达水平。结果:HH组的肺平均动脉压(mPAP)、WA/TA、RV/LV+SP明显高于C组,HH+LTZ组明显低于HH组(均P<0.01);3组的平均颈动脉压(mCAP)无明显差异(P>0.05)。TUNEL法测得HH组、HH+LTZ组的肺细小动脉凋亡指数(AI)显著低于C组(P<0.01),HH+LTZ组肺细小动脉凋亡指数显著高于HH组(P<0.05)。血浆硫化氢(H2S)含量、肺组织匀浆胱硫醚-γ-裂解酶(CSE)活性、肺组织CSE基因表达水平,HH组明显低于C组(P<0.01),HH+LTZ组明显高于HH组(P<0.01)。结论:川芎嗪可能通过上调CSE基因表达,增加CSE的活性,提高H2S水平,从而降低低O2高CO2性肺动脉高压。
AIM： To investigate the effect of sodium nitrite （SN） on lipopolysaccharide （LPS）-induced acute lung injury （ALI） and its underlying mechanism in mice. METHODS： All male Institute of Cancer Research （ICR） mice were randomly divided into five groups： Control group; LPS group; and SN 4.8 nmol/L, SN 48 nmol/L, SN 480 nmol/L （ip） groups. Lung wet weight/dry weight （W/D） ratio and permeability were detected. Neutrophil infiltration in bronchoalveolar lavage fluid （BALF） was measured by cel1 counting and morphological changes in lung tissues were assayed by hematoxylin-eosin staining. The 1evels of interleukin-10 （IL-10） and tumor necrosis factor-α （TNF-α） in lung were detected. Nitric oxide （NO） level and nitric oxide synthase （NOS） activity in lung were measured according to the specification. RESULTS： Compared to lung in LPS-induced ALI mice, at doses of 4.8 nmol/L and 48 nmol/L, not 480 nmol/L, SN markedly decreased the lung W/D ratio, total leukocyte number and neutrophil percentage in the BALF, lung permeability, and TNF-α/IL-10 ratio, in lung. SN at dose of 480 nmol/L markedly increased the lung NO level compared to control group. In addition, SN decreased the total NOS and inducible NOS （iNOS） activities compared to LPS-induced ALI mice. 〈BR〉CONCLUSION： These results indicate that the protective effect of SN against LPS-induced ALI in mice is associated with the low dose SN-induced NO, as well as the subsequent decrease in iNOS activity and TNF-α/IL-10 ratio.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2010年第3期524-528,共5页
Chinese Journal of Pathophysiology
基金
浙江省中医药科技计划资助项目(No.2007CA078)
温州市科技计划资助项目(No.Y20080183)
