Effects Of Actemera To IL-6and Survivin In Pulmonary Arterial Hypertension Rat Model

ObjectiveThe purpose of this paper was through the establishment of monocrotaline(MCT)-induced pulmonary arterial hypertension (PAH) rat models, to observethe effects of actemra to model pulmonary artery pressure, serum IL-6andsurvivin, to investigate the mechanism.Method1. the grouping method: experimental rats were divided into three groupsrandomly: A. The blank control group (n=10); B. The experimental control group(n=10); C. the actemra intervention group (n=10). Group A: Intraperitonealinjection of0.9%saline on the first day; Group B: Intraperitoneal injection ofMCT (60mg/kg) on the first day; Group C: intraperitoneal injection of MCT(60mg/kg) and actemra (5mg/kg) on the first day.2. Using the right heart microcatheter measure mean pulmonary arterypressure (mPAP) of the rat in each group.3. Observation of rat lung tissue and vascular stenosis (or vascular wallthickening) by HE staining.4. Observation expression of IL-6and survivin in pulmonary vascular byimmunohistochemical staining.5. Quantitative determination level of serum IL-6and survivin by ELISA,and comprehensive assessment of actemra on MCT induced PAH rat model.Results1. MPAP of rats: mPAP both in actemra intervention group and blank control group lower then experimental control group[(23.56±4.86) mmHg(19.14±4.30) mmHg vs.(41.71±8.79) mmHg, p<0.05. mPAP in actemraintervention group and control group was not statistically significant, p>0.05.2. HE staining showed that the experimental control group had markedthickening of the pulmonary vascular wall, surrounded by inflammatory cellinfiltration, had marked thickening of alveolar septa. Pulmonary artery intimalmild edema and mild thicken vessel wall in actemra intervention group.3. Immunohistochemistry showed strong expression of IL-6and survivin inthe lung tissue in the experimental control, a small amount of expression in ratlungs in actemra intervention group, and did not express in blank control group.4. ELISA quantitative determination of IL-6levels: actemra interventiongroup and control group was significantly lower than the experimental controlgroup [(1576.63±296.19) pg/ml,(1316.9798±71.20) pg/ml vs.(2069.49±295.60)pg/ml p<0.05]. Survivin levels: actemra intervention group and blank controlgroup was lower than the experimental control group [(12.22±1.11) ng/ml,(2.40±3.62) ng/ml vs.(43.32±8.16) ng/ml, p <0.05].Conclusions1. Actemra could inhibit MCT induced PAH effectively.2. The generation of PAH induced by MCT may be associated with IL-6signal transduction pathway.