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目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力的影响,探讨maFGF抗衰老的机制。方法选择成年Wistar大鼠40只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老对照组、NS对照组和maFGF治疗组。另10只不注射D-半乳糖作为正常对照组。maFGF治疗组按12μg/kg剂量肌内注射,1次/d,共14 d,NS对照组肌肉注射与maFGF治疗组相同容量的生理盐水,1次/d;衰老对照组不作任何干预。各组大鼠到相对应的时间点取出各组大鼠脑组织,测定脑组织匀浆中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力。结果与正常对照组相比,衰老对照组大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力均明显著降低(P<0.01);maFGF治疗组脑组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于衰老对照组、NS对照组(P<0.05)。结论 maFGF能升高衰老大鼠脑组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,对衰老大鼠脑损伤有一定保护作用。
Objective To observe the effect of modified acidic fibroblast growth factor (maFGF) on Na + -K + -ATPase activity and Ca2 + -Mg2 + -ATPase activity in brain tissue of D-galactose-induced senile rats and to explore the mechanism of maFGF anti-aging . Methods Forty adult Wistar rats were selected, and the aging model was established by subcutaneous injection of D-galactose. The aging model was randomly divided into aging control group, NS control group and maFGF treatment group. The other 10 were not injected D-galactose as a normal control group. The rats in the maFGF group were intramuscularly injected with 12 μg / kg once a day for 14 days. The NS control group was intramuscularly injected with the same volume of normal saline as the maFGF-treated group once a day, without any intervention in the aging control group. The rats in each group were sacrificed at the corresponding time points to take out 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 the brain tissue of aging rats were significantly decreased (P <0.01). In the maFGF treated group, Na + -K + -ATP enzyme activity and Ca2 + -Mg2 + -ATPase activity were significantly higher than the aging control group and NS control group (P <0.05). Conclusions maFGF can increase Na + -K + -ATPase activity and Ca2 + -Mg2 + -ATPase activity in brain tissue of senile rats, which may have a protective effect on brain injury in senile rats.