Inibição do receptor tipo-1 ativado por protease (PAR¹) na doença e reparo periodontal / Type 1 protease-activated receptor (PAR 1 ) inhibition on periodontal disease and repair

A sinalização celular por PAR¹ tem mostrado influenciar uma ampla gama de respostas patofisiológicas, incluindo ativação plaquetária, crescimento tumoral, inflamação e metástases. Baseando-se nisto, o objetivo do presente estudo foi avaliar o efeito do Parstatin, droga que tem ação biológica oposta àquela desencadeada pela ativação do PAR¹, durante o processo de indução e reparo da inflamação. Foi utilizado um modelo de periodontite experimental em ratos através da instalação de ligaduras de fio de algodão nos segundos molares superiores. Para isto, 72 ratos foram separados aleatoriamente em 9 grupos com 8 animais cada e receberam as ligaduras e injeção de veículo ou Parstatin nos períodos de 7 e 14 dias para observar a ação da inibição deste receptor nos períodos de indução de inflamação e reparo. Após estes períodos, os animais foram sacrificados e tiveram as maxilas removidas, dissecadas e divididas ao meio para avaliação histológica e radiográfica a fim de caracterizar infiltrado de células inflamatórias e perda óssea ao redor dos dentes.

PAR¹ cell signaling has been shown to be involved in several pathophysiological responses including platelet activation, tumor growth, inflammation and metastasis. Based on this, the aim of the present study was to evaluate the influence of Parstatin, a drug that presents a biological effect opposed to that of PAR¹ receptor activation, on inflammation induction and repair processes. Rats were subjected to cotton ligature-induced periodontitis bilaterally on the second upper molar teeth. Seventy-two rats were randomly assigned to 9 groups (n=8/group) and received ligatures and injection of vehicle or Parstatin for 7 or 14 days for both inflammation and repair induction. After that, the animals were sacrificed and their maxilla removed, dissected and divided in two for histologic and radiographic evaluation to characterize inflammatory cell infiltrate and bone loss around teeth.

Effect of low molecular weight heparin on the expression of endothelial protein C receptor and protease activated receptor 1 in abdominal aortic endothelial cells of septic rats / 中国医师杂志

Objective To investigate the effect of low molecular weight heparin (LMWH) on the expression of endothelial protein C receptor (EPCR) and protease activated receptor 1 (PAR1) in abdominal vascular endothelial cells (VECs) of septic rats. Methods VECs were cultured by tissue-sticking method, and the purity was determined with flow cytometry (FCM). VECs were randomly divided into three groups: control group, septic group (LPS 1 μg/ml) and LMWH group (LPS 1 μg/ml+LMWH 5 μg/ml). The VECs were collected at 1st, 3rd, 5th days after stimulated. The expression of EPCR and PAR1 were assessed by FCM. Results The expression of EPCR and PAR1 of septic group decreased significantly compared with control group at each time point (P＜0.05 or P＜0.01), and the expression decreased most obviously on day 5 (26.53±7.21 vs 39.26±2.62,q＝6.45,P＜0.01;53.21±15.10 vs 86.54±11.34,q＝6.94,P＜0.01). In LMWH group, the levels of EPCR and PAR1 expression were higher than setpic group at each time point (P＜0.05). Compared to control group, the expression of EPCR had a significantly decrease on day 1 (40.86±1.63 vs 45.41±2.82,q＝3.51,P＜0.05), which had no significantly different on day 3 and 5 (41.20±3.32 vs 42.83±2.66,P＞0.05;39.23±3.33 vs 39.26±2.62,P＞0.05), and the expression of PAR1 were not significantly decrease compared with control group at each time point (P＞0.05). Conclusions LMWH could improve the inhibition status and the expression of EPCR and PAR1 on VECs in septic rats.