补肾益精方延缓老年雄性大鼠骨与脑衰老的实验研究

作者	单位
张戈	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
马骏	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
张倩	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
史万忠	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
秦红友	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
宫斌	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
莫启忠	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032
石印玉	ZHANG Ge, MA Jun, ZHANG Qian, et al Institute of Orthopedics and Traumatology, Shanghai Academy of TMC, Shanghai (200032

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中文摘要:

目的 :评价补肾益精方延缓老年雄性大鼠骨衰老与脑衰老的作用 ,探讨此方延缓整个机体衰老的机制。方法 :4 0只 2 4月龄SD雄性大鼠随机分为 2 4月龄本底对照组、30月龄增龄对照组、补肾益精方低剂量组、补肾益精方高剂量组 ,每组各 10只。低剂量组、高剂量组均自 2 4月龄给药至 30月龄。各组相应处理以后分别测定各组大鼠的骨参数 (左侧股骨近段、中段、远段的骨密度和右侧股骨的弯曲断裂载荷 )以及脑参数 (脑组织M受体结合容量和胆碱酯酶活性 )。结果 :在骨方面 ,补肾益精方既能量效依赖性地增加大鼠股骨各段骨密度 ,又能量效依赖性地提高大鼠股骨弯曲断裂载荷 ;在脑方面 ,补肾益精方不仅能上调大鼠脑组织M受体结合容量 ,而且又能抑制大鼠脑组织胆碱酯酶活性。结论 :补肾益精方具有同时延缓雄性大鼠骨衰老与脑衰老的作用 ;推测该方似通过神经内分泌免疫网络的介导从整体角度调整衰老机体肾虚精亏之异常。

英文摘要:

Objective: To evaluate the effect of Bushen Yijing recipe (BSYJR) in delaying senility of bone and brain of aged male rats and infer its mechanism in delaying systemic senility. Methods: Forty male SD rats, 24 months old were randomly divided into 4 groups, the baseline control group, the aged control group (30 months old), the BSYJR high dose group and the BSYJR low dose group. The latter two groups received BSYJR treatment from 24 months old to 30 months old. Bone indexes (bone density of the proximal, middle and distal segments of left femur and break bending load of right femur) and brain indexes (binding capacity of M receptor and cholinesterase activity of brain) were measured after responding treatment. Results: In bone, BSYJR could not only increase the bone mineral density in various segments of femur, but also raise the bending break load of femur dose effect dependently. In brain, BSYJR could both up regulate the binding capacity of M receptor and inhibit the activity of cholinesterase. Conclusion: BSYJR could delay the senility of bone and brain in male rats, inferring that it might regulate integrally the abnormality of aging in Kidney Asthenia and Essence Deficiency through mediation of nerve endocrine immunity network.

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