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目的观察川芎嗪干预对新生大鼠高氧肺损伤的影响及可能作用机制。方法 80只足月新生12 h内的清洁级SD大鼠,随机分为空气组(A组)、空气+川芎嗪组(B组)、高氧(60%)组(C组)、高氧+川芎嗪组(D组)。B、D两组每日腹腔注射川芎嗪30 mg/kg,一日一次,A、C两组每日腹腔注射等量生理盐水,实验第14天每组随机选取8只,测量体重后取肺组织,测量肺质量,HE染色观察肺组织病理改变并计算其放射状肺泡计数(RAC)、RT-PCR方法检测内皮型一氧化氮合酶(eNOS)mRNA表达水平;免疫组织化学染色法检测eNOS蛋白表达水平。结果C组显示明显的肺泡发育受阻,体重(g)、肺质量(g)、RAC值(个)较A、B组均明显减少[体重:(17.4±3.2)比(29.5±1.7)、(29.3±1.6),肺质量:(0.26±0.04)比(0.41±0.03)、(0.40±0.03),RAC值:(4.8±0.7)比(9.0±0.8)、(8.8±0.9),P<0.05],D组病理改变减轻,体重、肺质量、RAC值高于C组(P<0.05),与A组相近(P>0.05)。与A组(3.54±0.37)相比,C组肺组织eNOS表达水平(2.76±0.23)明显降低,D组(3.80±0.36)表达较C组增加,差异有统计学意义(P<0.05),与A组相近(P>0.05)。结论高氧可导致新生大鼠出现肺损伤,病理改变类似于早产儿新型支气管肺发育不良,川芎嗪干预对其有一定保护作用,其机制可能与川芎嗪促进eNOS的表达并通过内源性NO生成增多而降低肺微血管压力有关。
Objective To observe the effect of ligustrazine on hyperoxia - induced lung injury in neonatal rats and its possible mechanism. Methods Totally 80 SD rats were divided into three groups randomly: air group (group A), air + ligustrazine group (group B), hyperoxia group (group C), hyperoxia group + Ligustrazine group (D group). The rats in groups B and D were injected intraperitoneally with ligustrazine 30 mg / kg once daily. The rats in groups A and C were injected intraperitoneally with equal volume of normal saline. On the 14th day, eight rats were randomly selected from each group. The pathological changes of lung tissue were observed by HE staining and the radial alveolar count (RAC) was calculated. The expression of eNOS mRNA was detected by RT-PCR. The expression of eNOS protein was detected by immunohistochemical staining The expression level. Results In group C, obvious alveolar development was blocked. Body weight (g), lung mass (g) and RAC value were significantly lower than those in group A and B [body weight: (17.4 ± 3.2) vs 29.5 ± 1.7 (P <0.05), P <0.05, P <0.05). The lung mass was significantly higher than that of the control group (P <0.05) ]. The pathological changes in group D were alleviated. The body weight, lung mass and RAC were higher in group C than in group C (P <0.05), similar to group A (P> 0.05). Compared with group A (3.54 ± 0.37), eNOS expression in group C (2.76 ± 0.23) was significantly lower than that in group A (3.80 ± 0.36), and the difference was statistically significant (P <0.05) Similar to group A (P> 0.05). Conclusion Hyperbaric oxygen can cause lung injury in neonatal rats. The pathological changes are similar to the new type of bronchopulmonary dysplasia in premature infants. Ligustrazine can protect the neonatal rats from the pathogenesis. The mechanism may be that ligustrazine can promote the expression of eNOS, Increased production and lower pulmonary microvascular pressure.