Zhang Hong-min, Chen Shi-wei, Xie Chun-guang, Xie Yi-qiang, Deng Xi-fang
Department of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu.
Zhongguo Zhong Yao Za Zhi. 2006 Aug;31(15):1272-6.
To explore the mechanism of Shenqi compound recipe (SQCR) anti-earlier diabetic artherosclerosis in GK rats.
Four-month specefic pathogen free (SPF) GK rats were divided randomly according to blood glucose level into four groups: model group (5 mL x kg(-1) x d(-1) sterile water), ramipril group (positive control, 1 mg x kg(-1) x d(-1)), SQCR low dosage (0.72 g x kg(-1) x d(-1)) and SQCR high dosage group (2.88 g x kg(-1) x d(-1)) and Wistar rats as normal control group(5 mL x kg(-1) x d(-1) sterile water). GK rats took high-fat diet freely and meanwile were injected N-omega-nitro-L-arginine methyl ester (L-N-AME) intra-peritoneally with the dose of 10 mg x kg(-1) x d(-1) in order to induce earlier diabetic artherosclerosis, while normal control group took regular diet and were injected normal saline intra-peritoneally. In the experiment periods, each group was administrated correspondent substance respectively for 32 d. At the end, sampling blood by abdominal aorta and picking aorta on ice. Determined monocyte chemoattractant protein-1 (MCP-1) concentration by ELISA, messenger ribonucleic acid (mRNA) expression of MCP-1 and peroxisome proliferator-activated receptor gamma (PPARgamma) in aorta by reverse transcriptase PCR (RT-PCR).
Concentrations of MCP-1 in serum in SQCR low and high dosage groups and the mRNA expression of MCP-1 in SQCR high dosage group were all decreased significantly compared with model group (P < 0.05). The mRNA expression of PPARgamma in SQCR low and high dosage groups all increased compared with model group (P < 0.05 or P < 0.01).
Inhibiting the mRNA and protein expression of MCP-1 and upregulating the mRNA expression of PPARgamma in aorta might be contribute to SQCR anti-earlier diabetic artherosclerosis in GK rats partly.
探讨参芪复方（SQCR）抗GK大鼠早期糖尿病动脉粥样硬化的机制。
将4月龄无特定病原体（SPF）的GK大鼠按血糖水平随机分为4组：模型组（5 mL·kg⁻¹·d⁻¹无菌水）、雷米普利组（阳性对照，1 mg·kg⁻¹·d⁻¹）、SQCR低剂量组（0.72 g·kg⁻¹·d⁻¹）和SQCR高剂量组（2.88 g·kg⁻¹·d⁻¹），以Wistar大鼠作为正常对照组（5 mL·kg⁻¹·d⁻¹无菌水）。GK大鼠自由摄食高脂饲料，同时腹腔注射剂量为10 mg·kg⁻¹·d⁻¹的N-ω-硝基-L-精氨酸甲酯（L-N-AME）以诱导早期糖尿病动脉粥样硬化，而正常对照组给予常规饲料并腹腔注射生理盐水。在实验期间，每组分别给予相应物质32天。实验结束时，经腹主动脉采血并在冰上摘取主动脉。采用酶联免疫吸附测定（ELISA）法测定单核细胞趋化蛋白-1（MCP-1）浓度，采用逆转录聚合酶链反应（RT-PCR）法检测主动脉中MCP-1和过氧化物酶体增殖物激活受体γ（PPARγ）的信使核糖核酸（mRNA）表达。
与模型组相比，SQCR低、高剂量组血清中MCP-1浓度及SQCR高剂量组主动脉中MCP-1的mRNA表达均显著降低（P < 0.05）。与模型组相比，SQCR低、高剂量组主动脉中PPARγ的mRNA表达均升高（P < 0.05或P < 0.01）。
抑制主动脉中MCP-1的mRNA和蛋白表达以及上调PPARγ的mRNA表达可能是参芪复方抗GK大鼠早期糖尿病动脉粥样硬化的部分作用机制。
