丹参对自发性高血压大鼠左室肥厚及心肌肿瘤坏死因子表达影响

The Effect of Salvia Miltiorrhiza Bge on Left Ventricular Hypertrophy and the Expression of Tumor Necrosis Factor-α in Spontaneously Hypertensive Rats

目的 观察丹参对自发性高血压大鼠左室肥厚作用及左室心肌肿瘤坏死因子 (TNF α)的影响 ,并探讨其作用机制。方法 实验用WKY大鼠做阴性对照组 ,SHR大鼠分为对照组和治疗组。治疗组给予丹参注射液腹腔内注射 12周 ,其余两组分别注射相当容积的蒸馏水。测量大鼠尾动脉收缩压 (SBP)及左心室重量指数 (LVMI)。应用HE、VG染色、免疫组织化学的方法 ,结合计算机图像分析技术 ,检测心肌细胞的直径和面积、心肌组织胶原体积比例 (CVF)、血管周围胶原面积和管腔面积比例 (PVCA)以及左心室心肌TNF α表达。结果 与WKY大鼠相比 ,2 0周龄SHR大鼠的SBP、LVMI、心肌细胞的直径、面积、CVF、PVCA显著增加 ,TNF α表达上调 ,用丹参治疗后 ,SHR除收缩压外余指标均显著性下降 (P <0 0 5 )。结论 长期应用丹参治疗可预防和逆转高血压大鼠左室肥厚形成 ,其机制可能与丹参降低心肌TNF

Objective To study the effect of Salvia Miltiorrhiza Bge(SMB) on left ventricular hypertrophy(LVH)and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle in spontaneously hypertensive rats. Methods Normal Wistar-Kyoto(WKY)-rats were used as negative control, and spontaneously hypertensive rats(SHR) were randomly to receive placebo or Salvia Miltiorrhiza Bge(SMB). SMB (1 g/kg·d) were injected intraperitoneally for 12 weeks. Systolic blood pressure (SBP)and left ventricular mass index(LVMI)were measured. HE, VG and immunohistochemical staining combined with computed morphometry were employed to evaluate the cardiomyocyte size, diameter, the collagen volume fraction(CVF), perivascular circumferential area(PVCA), and tumor necrosis factor-α (TNF-α)expression in the left ventricular tissue. Results Compared with WKY rats, the SBP, LVMI, cardiomyocyte size, diameter, CVF, PCVA, and TNF-α expression increased markedly in the 20-week-old spontaneously hypertensive rats. SMB decreased LVMI(4.5±0.3 mg/g vs SHR 4.9±0.4 mg/g, P<0.01), size of cardiomyocytes(231.2±69.3 μm 2 vs SHR 490±118.9 μm 2, P<0.01), collagen volume fraction(4.7%±1.0% vs SHR 7.9%±0.8%, P<0.01), perivascular circumferential area(2.95%±0.57% vs SHR 4.85%±0.6%, P<0.01), and TNF-α expression(0.14±0.04 vs SHR 0.18±0.02 OD, P<0.01) with no effect on SBP (191±31 mmHg vs SHR 205±26 mmHg). Conclusion Chronic administration of SMB inhibit and regress the development of LVH in spontaneously hypertensive rats independent of BP. TNF-α may be involved in the reversal mechanism of LVH by SMB.