Objective To investigate the effects of pulmonary artery denervation (PADN)on pulmonary artery function outside of the nervous system.Methods Thirty-six beagles of 8-10 months old weighting 8-15 kg were randomized into six groups:a blank control group,an immediate post-surgery group,a 1 month post-surgery group,a 2 months post-surgery group,a 3 month post-surgery group,and a pulmonary artery hypertension(PAH)group,with six dogs in each group.Dogs in the blank control group received no treatment,and dogs in the surgery groups were treated with PADN and were then killed immediately after surgery,at 1,2 or 3 months after surgery.PAH dogs were induced by dehydromonocrotaline,and they were killed at 8 weeks after treatment.Protein levels of angiotensin Ⅱ (Ang Ⅱ),angiotensin converting enzyme (ACE),angiotensin converting enzyme 2 (ACE2),mineralocorticoid receptors (MR)and antibodies against aldosterone in dog pulmonary and right ventricular tissues were detected by Western blot.The mRNA expression of the Ang Ⅱ type 1 receptor(AT1R)was determined by real-time reverse transcription quantitative polymerase chain reaction(RT-qPCR).The protein expression ratio of ACE2 to ACE in lung and right ventricular tissues were calculated.Changes of the renin-angiotensin-aldosterone system (RAAS)in lung and right ventricular tissues were compared between the groups.Results In pulmonary tissues,protein levels of Ang Ⅱ,ACE2,MR,and AT-1R increased immediately after PADN (P =0.03,0.03,0.01 and ＜ 0.01),and the protein expression of ACE decreased(P ＜0.001),indicating that RAAS was activated immediately after PADN.Three months after PADN,Ang Ⅱ protein levels declined significantly in lung tissues(P =0.030),and ACE2,ACE,MR,and AT-1 receptor protein expression had no obvious difference(P =0.670,0.570,0.180 and 0.349),compared with the blank control group.In right ventricular tissues,the protein expression of ACE2 was higher in the surgery groups than in the blank control group(P =0.0161),and there was no significant difference in the protein expression of Ang Ⅱ,ACE,MR,and AT-1 receptors(P=0.641,0.134,0.227 and 0.330).Conclusions RAAS activates immediately in dogs with normal pulmonary pressure after PADN,the damaging factors in pulmonary tissues are reduced and the vascular protective factors in right ventricular tissues are elevated at 3 months after PADN.

Objective: To investigate blood pressure and vascular remodeling of OSAS by establishing the chronic-intermittent hypoxia model in rat. Methods: Experiments were performed on 35 adult male Sprague-Dawley rats. Animals were randomly divided into four groups: unhandled control group (with 5 rats in it), CIH group at 9/6/3 weeks (with 10 ratsin each group). Rats in CIH group went through 8-hour intermittent hypoxia everyday, and those in control group were raising normally. After 9-week experiment, blood pressure was measured. The changes of the following indexes were observed: pathological changes of aorta and the middle aorta thickness (HE staining), the collagen of aorta wall (Masson staining). The experimental data were analyzed by SPSS 24.0 statistical software. The variance was analyzed by one-way analysis of variance, and the irregularity was selected using the calibration t test. Results: The systolic and diastolic blood pressures of the CIH9, 6, and 3 weeks groups and the control group were: (127±13) and (79±9), (124±11) and (81±7), (101±11) and (75±9), (91±10) and (65±9) mmHg (1 mmHg=0.133 kPa). The systolic blood pressure and diastolic blood pressure of the rats in the week of CIH 9 and 6 weeks were significantly higher than the control group (F=14.64, P=0.000; F=6.81, P=0.000). There was no significant difference in the mean blood pressure between the three groups of CIH and the control group. Membrane thickness in CIH9, 6 and 3 weeks and control group were: (20±2), (19±2), (14±2), (13±3) μm. Compared with the control group, the aortic pathology and thickness of the middle layer of the CIH9 and 6 weeks group were significantly thicker (F=20.24, P=0.000), but there was no significant difference between the CIH3 week group and the control group; the collagen deposition was unchanged compared with the control group. Conclusion Intermittent hypoxia for 6 weeks or more in rats resulted in the increasement of blood pressure, morphological changes of aorta and vascular remodeling in thickened media.

Objective: To investigate the role of p38 MAPK pathway in IL-1β induced inflammatory secretory properties mesenchymal stem cells(SFMSCs) from human synovial fluid of temporomandibular joint. Methods: In vitro cultured hSFMSCs were divided into control group and IL-1β treated group(10 ng/ml IL-1β for 2 h), the activation of p38 MAPK was examined with western blot. Then, the gene expression and the secretion of IL-6 and IL-8 in control group, IL-1β treated group and p38 MAPK inhibitor pre-treated group(pretreatment with SB-203580 10 μmol/L prior to the addition of 10 ng/ml IL-1β) were examined by RT-PCR and cytometric bead array(CBA). Results: It was observed that the protein level of p-p38 MAPK, the secretion of IL-8 and IL-6 were increased in IL-1β treated group, and suppressed in p38 MAPK inhibitor pre-treated group. Conclusion: p38 MAPK pathway of SFMSCs might play a role in IL-6 and IL-8 secretion by SFMSCs in inflammatory environment.