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目的观察碱性成纤维细胞生长因子(bFGF)对慢性酒精中毒大鼠脑组织Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力,探讨bFGF对慢性酒精中毒所致的脑损伤的保护作用。方法选择成年Wistar雄性大鼠,采用白酒灌胃建立慢性酒精中毒模型,慢性酒精中毒模型建立成功的大鼠随机抽签法分为酒精中毒对照组、生理盐水(NS)对照组和bFGF治疗组。另10只不灌白酒作为正常对照组。bFGF治疗组大鼠白酒灌胃的同时,1h后按12g/kg剂量肌肉注射,共14d。各组大鼠到相对应的时间点取出各组大鼠脑组织制成匀浆,测定脑组织匀浆中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力。结果与正常对照组相比,慢性酒精中毒后大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力均明显降低(P<0.01);经bFGF治疗后脑组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于酒精中毒对照组及NS对照组(P<0.05)。结论 bFGF能提高慢性酒精中毒脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,提示bFGF对慢性酒精中毒所致的脑损伤具有保护作用。
Objective To observe the effect of basic fibroblast growth factor (bFGF) on Na + -K + -ATPase activity and Ca2 + -Mg2 + -ATPase activity in brain tissue of rats with chronic alcoholism and to explore the protective effect of bFGF on brain injury induced by chronic alcoholism . Methods Adult Wistar male rats were randomly divided into alcohol poisoning control group, NS control group and bFGF treatment group. The model of chronic alcoholism was established by gavage with alcohol. The model of chronic alcoholism was established successfully. The other 10 do not fill the liquor as a normal control group. Rats in bFGF treatment group were given intragastric administration of gin at the same time, and were injected intramuscularly at a dose of 12g / kg after 1h for 14 days. The rats in each group were sacrificed at the corresponding time points to take out the homogenates of the brain tissue of rats in each group. The activities of Na + -K + -ATPase and Ca2 + -Mg2 + -ATPase in brain homogenate were measured. Results Compared with the normal control group, Na + -K + -ATPase activity and Ca2 + -Mg2 + -ATPase activity in brain tissue of rats with chronic alcoholism were significantly decreased (P <0.01). After bFGF treatment, Na + -K + -ATP enzyme activity and Ca2 + -Mg2 + -ATPase activity were significantly higher than those in alcohol poisoning control group and NS control group (P <0.05). Conclusion bFGF can increase Na + -K + -ATPase activity and Ca2 + -Mg2 + -ATPase activity in brain tissue of chronic alcoholism, suggesting that bFGF has a protective effect on brain injury induced by chronic alcoholism.