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阿利吉仑减轻患有牙周病的糖尿病小鼠的炎症反应和伤口愈合过程。

Aliskiren Attenuates the Inflammatory Response and Wound Healing Process in Diabetic Mice With Periodontal Disease.

作者信息

Oliveira Sandra Helena Penha, Brito Victor Gustavo Balera, Frasnelli Sabrina Cruz Tfaile, Ribeiro Bianca da Silva, Ferreira Milena Nunes, Queiroz Dayane Priscilla, Beltan Carluci Taís, Lara Vanessa Soares, Santos Carlos Ferreira

机构信息

Department of Basic Sciences, School of Dentistry of Araçatuba, São Paulo State University (UNESP), São Paulo, Brazil.

Programa Multicêntrico de Pós-graduação em Ciências Fisiológicas, School of Dentistry of Araçatuba, São Paulo State University (UNESP), São Paulo, Brazil.

出版信息

Front Pharmacol. 2019 Jul 4;10:708. doi: 10.3389/fphar.2019.00708. eCollection 2019.

Abstract

The aim of this study was to characterize the role of local RAS (renin-angiotensin system) in the inflammatory response of normal (N) and diabetic (D) mice with periodontal disease (PD). Diabetes Mellitus (DM) was induced by peritoneal injection of streptozotocin in Balb/c mice. PD was induced by ligature around the first molar in both N and D, irrespective of whether they were treated with aliskiren (50 mg/kg, Alisk). Mandibles were harvested for histomorphometric analyses, and gingival tissue (GT) was collected to evaluate gene expression and extracellular matrix components (ECM). Immunohistochemical (IHC) analyses were used to localize RAS in GT. The production of C-reactive protein (CRP), IL-1β, CXCL2, and CCL8 was evaluated by enzyme-linked immunosorbent assay (ELISA). Renin was found to exacerbate the inflammation and periodontal bone loss at 14 days after PD, and Alisk inhibited this process in GT of N and D. PD increased CRP, CXCL2, CCL8, and IL-1β production in both animals. Alisk could inhibit CRP, CXCL2, and CCL8 primarily in D animals. However, only CCL8 was decreased in N animals after Alisk pretreatment. PD enhanced expression and production of AGT, ACE, AT1R, and AT2R in both N and D. AT1R expression was higher in D with PD, and AT2R expression was higher in N with PD. ACE2 and receptor Mas (MasR) expression and production was elevated in the control group of both animals. PD inhibited ACE2 in N but not in D. MasR expression was unaffected in both N and D with PD. Alisk reduced expression and production of all RAS components in GT of both animals, except for ACE2 in N. RAS staining was observed in all layers of epithelium, basal cell layer, and lamina propria and was higher in N with PD. Col1a1, Col1a2, Col3a1, and fibronectin (Fn1) were increased in both animals with PD. Alisk inhibited Col1a1 and Fn in both animals, Col1a2 was decreased only in D, while levels of Col3a1 remained unchanged in all animal groups. In conclusion, these data demonstrated the presence and functional role of local RAS in GT, exacerbating the inflammatory response, periodontal bone loss, and wound healing processes in both N and D animal groups. In addition, Alisk was able to significantly reduce gingival inflammation, excessive wound healing processes, and periodontal bone loss.

摘要

本研究的目的是确定局部肾素-血管紧张素系统(RAS)在患有牙周病(PD)的正常(N)小鼠和糖尿病(D)小鼠炎症反应中的作用。通过腹腔注射链脲佐菌素诱导Balb/c小鼠患糖尿病。无论N组和D组小鼠是否接受阿利吉仑(50 mg/kg,Alisk)治疗,均通过结扎第一磨牙诱导牙周病。采集下颌骨进行组织形态计量学分析,并收集牙龈组织(GT)以评估基因表达和细胞外基质成分(ECM)。采用免疫组织化学(IHC)分析在GT中定位RAS。通过酶联免疫吸附测定(ELISA)评估C反应蛋白(CRP)、白细胞介素-1β(IL-1β)、CXC趋化因子配体2(CXCL2)和C-C趋化因子配体8(CCL8)的产生。发现肾素在PD后14天加剧炎症和牙周骨丢失,而Alisk在N组和D组的GT中抑制了这一过程。PD增加了两组动物中CRP、CXCL2、CCL8和IL-1β的产生。Alisk主要在D组动物中抑制CRP、CXCL2和CCL8。然而,Alisk预处理后,N组动物中只有CCL8减少。PD增强了N组和D组中血管紧张素原(AGT)、血管紧张素转换酶(ACE)、血管紧张素Ⅱ1型受体(AT1R)和血管紧张素Ⅱ2型受体(AT2R)的表达和产生。患有PD的D组中AT1R表达较高,患有PD的N组中AT2R表达较高。两组动物的对照组中血管紧张素转换酶2(ACE2)和Mas受体(MasR)的表达和产生均升高。PD抑制了N组中的ACE2,但未抑制D组中的ACE2。PD状态下,N组和D组中MasR的表达均未受影响。Alisk降低了两组动物GT中所有RAS成分的表达和产生,但N组中的ACE2除外。在所有上皮层、基底细胞层和固有层均观察到RAS染色,且患有PD的N组中染色更强。患有PD的两组动物中Ⅰ型胶原α1(Col1a1)、Ⅰ型胶原α2(Col1a2)、Ⅲ型胶原α1(Col3a1)和纤连蛋白(Fn1)均增加。Alisk抑制了两组动物中的Col1a1和Fn,Col1a2仅在D组中减少,而Col3a1水平在所有动物组中均保持不变。总之,这些数据证明了GT中局部RAS的存在及其功能作用,加剧了N组和D组动物的炎症反应、牙周骨丢失和伤口愈合过程。此外,Alisk能够显著减轻牙龈炎症、过度的伤口愈合过程和牙周骨丢失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e57e/6620569/f186d5c284e7/fphar-10-00708-g001.jpg

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