Li Jinqi, Peng Cheng, Ji Jieying
Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China.
Zhongguo Zhong Yao Za Zhi. 2009 Nov;34(22):2937-42.
To investigate the mechanism of action on compatible using of total alkaloids of Radix Aconiti Praeparata and total glycosides or polysaccharides of Radix Paeoniae Alba therapy on rheumatoid arthritis in rats.
The rat models of rheumatoid arthritis of cold and dampness syndrome were treated with total alkaloids of Radix Aconiti Praeparata and total glycosides or polysaccharides of Radix Paeoniae Alba. Observed the contents of hypothalamic L-ENK, hypothalamic-END, plasmatic SP, serumal IgG, serumal cell factors (IL-1beta, TNF-alpha, IL-6, IL-2, IL-10) by radioimmunity method and ultrastructural change of synovial cell in electron microscope.
Total alkaloids of Radix Aconiti Praeparata and total glycosides or polysaccharides of Radix Paeoniae Alba could relieve arthrocele and arthralgia and elevate the contents of L-ENK, beta-END, IL-2 and degrade the contents of SP, IgG, IL-1beta, IL-6 and inhibit abnormal secretion accentuation of synovial cell like fiber.
Total alkaloids of Radix Aconiti Praeparata and total glycosides or polysaccharides of Radix Paeoniae Alba could be used to treat rheumatoid arthritis of cold and dampness syndrome. The mechanism of action might be that the contents of center endogenous opioid peptides had increased, the synthesis and release of SP had been inhibited, the disturbance of serumal cell factor had been adjusted, and the synthesis and secretion of serum immune globulin and abnormal secretion accentuation of synovial cell had been inhibited.
探讨制川乌总生物碱与白芍总苷或白芍总多糖配伍治疗大鼠类风湿关节炎的作用机制。
用制川乌总生物碱与白芍总苷或白芍总多糖治疗大鼠寒湿痹阻型类风湿关节炎模型,采用放射免疫法观察下丘脑亮氨酸脑啡肽(L-ENK)、下丘脑内啡肽(END)、血浆P物质(SP)、血清免疫球蛋白G(IgG)、血清细胞因子(白细胞介素1β、肿瘤坏死因子α、白细胞介素6、白细胞介素2、白细胞介素10)含量,并用电镜观察滑膜细胞超微结构变化。
制川乌总生物碱与白芍总苷或白芍总多糖能减轻关节肿胀和疼痛,提高L-ENK、β-END、IL-2含量,降低SP、IgG、IL-1β、IL-6含量,抑制滑膜细胞如纤维样异常分泌亢进。
制川乌总生物碱与白芍总苷或白芍总多糖可用于治疗寒湿痹阻型类风湿关节炎。其作用机制可能是中枢内源性阿片肽含量增加,抑制了SP的合成与释放,调节了血清细胞因子紊乱,抑制了血清免疫球蛋白的合成与分泌及滑膜细胞异常分泌亢进。