Huang Xiao-ying, Xu Xiao-mei, Qian Guo-qing, Wang Liang-xing
Department of Respiration, The First Hospital of Wenzhou Medical College, Wenzhou 325003, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2010 May;26(2):217-21.
To study the effect and mechanism of chimonin on pulmonary arterioles I and III type collagen metabolism in pulmonary hypertension rats induced by chronic hypoxic hypercapnia.
Thirty-six Sprague-Dawley rats were randomly divided into three groups: normal control group(A), hypoxic hypercapnic group(B), hypoxic hypercapnia + chimonin group(C). Collagen I, III and their mRNA, Blood CO concentration (COHb%), activity of HO-1 in blood serum and lung homogenate, content of hydroxyproline in lung homogenate, pulmonary arteriole micromorphometric index were observed.
Hypoxic hypercapnic rats's mPAP, Hyr of lung homogenate, content of I type collagen and I type collagen mRNA in pulmonary arterioles, were significantly higher than those in control group, pulmonary vessel remodeling of hypoxic hypercapnic rats was significant, those changes in hypercapnia + chimonin group were significantly lower than those in hypoxic hypercapnic group. Blood CO concentration, activity of HO-1 in blood serum and lung homogenate in rats of hypoxic hypercapnic rats were significantly higher than those of control group, and those of hypercapnia + chimonin group were even higher than hypoxic hypercapnic group (P < 0.01). There was no significant difference in mCAP, content of III type collagen and their mRNA in three groups (P > 0.05).
Chimonin can reduce pulmonary hypertension and pulmonary vessel remodeling induced by hypoxic hypercapnia through inhibiting proliferation of collagen I, the mechanism maybe is up regulating endogenous carbon monoxide system.
研究知母宁对慢性低氧高碳酸血症诱导的肺动脉高压大鼠肺小动脉Ⅰ型和Ⅲ型胶原代谢的影响及其机制。
将36只Sprague-Dawley大鼠随机分为三组:正常对照组(A组)、低氧高碳酸血症组(B组)、低氧高碳酸血症+知母宁组(C组)。观察各组大鼠肺小动脉Ⅰ型和Ⅲ型胶原及其mRNA、血中碳氧血红蛋白(COHb%)、血清和肺匀浆中血红素加氧酶-1(HO-1)活性、肺匀浆中羟脯氨酸含量、肺小动脉形态计量学指标。
低氧高碳酸血症大鼠的平均肺动脉压(mPAP)、肺匀浆羟脯氨酸含量、肺小动脉Ⅰ型胶原含量及Ⅰ型胶原mRNA均显著高于对照组,低氧高碳酸血症大鼠肺血管重塑明显,低氧高碳酸血症+知母宁组上述改变明显低于低氧高碳酸血症组。低氧高碳酸血症大鼠血中CO浓度、血清和肺匀浆中HO-1活性显著高于对照组,低氧高碳酸血症+知母宁组更高于低氧高碳酸血症组(P<0.01)。三组大鼠的平均毛细血管压(mCAP)、Ⅲ型胶原含量及其mRNA差异无统计学意义(P>0.05)。
知母宁可通过抑制Ⅰ型胶原增生减轻低氧高碳酸血症所致的肺动脉高压及肺血管重塑,其机制可能与上调内源性一氧化碳系统有关。