利血平致脾虚大鼠唾液蛋白分泌改变及其机制的探讨

目的观察利血平致脾虚大鼠唾液蛋白分泌的改变并探讨其机制。方法利血平组大鼠20只皮下注射0.4mg/(kg.d)利血平9d造模,对照组大鼠20只注射生理盐水9d;10d时两组各随机抽取10只大鼠检测酸刺激前后唾液淀粉酶活性(sAA)比值,眼眶静脉采血检测血清的血管活性肠肽(VIP)和环磷酸腺苷(cAMP),处死动物取腮腺检测VIP和cAMP,取腮腺HE染色病理组织学观察和透射电镜计数腮腺酶原颗粒。两组剩余大鼠均停止注射并正常饲养40d,检测以上项目。结果利血平组大鼠较对照组食量明显减少、体重下降。10d时:利血平组sAA活性比值(0.39±0.18)显著低于对照组(0.80±0.21,P0.01),25d已恢复正常并持续至40d(与本组10d比较,P0.05;与对照组比较,P0.05);HE染色病理组织学检查未见两组腮腺有明显病理改变,透射电镜发现利血平组的单位观察视野腮腺酶原颗粒数(41.4±4.9)高于对照组(34.6±5.2,P0.01);血清VIP利血平组(22.5±13.1mg/L)低于对照组(38.5±14.1mg/L,P0.05),腮腺VIP两组差异无统计学意义;血清cAMP利血平组(125.8±15.5μmol/L)高于对照组(105.3±16.7μmol/L,P0.05),腮腺cAMP两组差异无统计学意义。40d时各项检测指标两组比较差异无统计学意义。结论利血平致脾虚大鼠酸刺激下唾液蛋白分泌减少,可能与VIP和cAMP调节途径有关。

Effect and Mechanism of Reserpine for Changing Salivary Protein Secretion in Pi-deficient Rats

Objective To study the effect of reserpine （RSP） for changing salivary protein secretion in Pi-deficient rats and to explore its possible mechanism. Methods Twenty rats allocated in the RSP group were given subcutaneous injection of RSP 0.4 mg/（kg·d） for 9 successive days, while the other 20 rats in the control group were injected with same volume of saline instead. On the 10th day, ten rats randomly selected from each group were subjected for extracting saliva to detect salivary amylase activity （sAA） before and after an acid stimulation; and drawing blood from the orbital vein to measure the contents of vasoactive intestinal peptide （VIP） and cyclic adenosine monophosphate （cAMP）. Then they were sacrificed and their parotids were taken out for pathological examination with HE staining, as well as for VIP and cAMP measuring, and zymongen granules counting under a transmission electron microscope. The remainder animals were stopped injecting and normally fed to 40 days, then subjected to be detected as above-mentioned. Results Food intake and body weight reduction were more significantly in the RSP group than in the control group. On the 10th day, the ratio of sAA before/after stimulation in the RSP group was 0.39±0.18, significantly lower than that in the control group （0.80±0.21, P〈0.01）, but it was restored rapidly, reaching the normal range on the 25th day, on the 40th day, it became significantly different to the level on the 10th day （P〈0.05） and approached the level in the control group （P〉0.05）. No significant pathological change of parotid was found in both groups; but the number of zymongen granules in the RSP group was remarkably more than that in the control group （41.4±4.9 vs 34.6±5.2, P〈0.01）. Serum level of VIP in the RSP group was significantly less while that of cAMP was higher than that in the control group （22.5±13.1 mg/L vs 38.5±14.1 mg/L, and 125.8±15.5 μmol/L vs 105.3±16.7 μmol/L, both P〈0.05）, but no inter-group difference was found in parotid tissue contents of both VIP and cAMP. All the indices detected became equivalent in the two groups on the 40th day. Conclusion The reduction of salivary protein in Pi-deficient rats induced by RSP may be related to the regulatory pathway of VIP and cAMP.