膜联蛋白A1/FPR2通路在雌激素缺乏雌性糖尿病大鼠牙槽骨细胞COX2/NLRP3炎性体调控中的可能作用

IF 4.2 2区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
Gisela Rodrigues Da Silva Sasso, Paulo Sérgio Cerri, Estela Sasso-Cerri, Manuel Jesus Simões, Cristiane Damas Gil, Rinaldo Florencio-Silva
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引用次数: 0

摘要

背景:膜联蛋白A1 (ANXA1)和nod样受体家族pyrin结构域蛋白3 (NLRP3)炎性体在骨重塑中发挥重要作用。然而,在糖尿病(DM)和雌激素缺乏的情况下,这些因子在骨细胞中的表达谱知之甚少。本研究研究了糖尿病和雌激素缺乏大鼠肺泡过程重构过程中ANXA1及其甲酰基肽受体2 (FPR2)以及NLRP3炎症小体介质的免疫表达。方法:将20只成年雌性Wistar大鼠分为4组(n = 5):假手术(SHAM)和去卵巢(OVX)大鼠给予载药液,假手术(SHAM)和去卵巢(OVX)大鼠分别腹腔注射链脲佐菌素(STZ) 60 mg/kg/体重(BW)诱导DM (SHAM- di组和OVX- di组)。7周后处死大鼠,用4%甲醛磷酸盐缓冲液固定上颌骨,石蜡包埋。切片采用苏木精/伊红(H&E)和小红染色或免疫组化检测ANXA1、FPR2、NLRP3、白细胞介素-1β (IL-1β)和环氧化酶-2 (COX2)。结果:雌激素缺乏和糖尿病与骨组织的有害影响有关,与非糖尿病组相比,SHAM-Di和OVX-Di组骨细胞数量减少,空腔隙数量增加。两组患者牙槽骨组织血管面积减小,胶原纤维双折射强度减弱。在糖尿病和OVX组中,尤其是在雌激素缺乏和糖尿病大鼠中,ANXA1/ fpr2阳性的成骨细胞、骨细胞和破骨细胞数量显著增加,同时这些细胞免疫标记为COX2、NLRP3和IL-1β的数量显著增加。结论:这些结果表明,在雌激素缺乏和糖尿病的骨重塑过程中,ANXA1/FPR2通路可能作为一种微调/抗炎调节剂,抵消骨细胞中COX2/NLRP3/IL-1β活化的加剧。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Possible role of annexin A1/FPR2 pathway in COX2/NLRP3 inflammasome regulation in alveolar bone cells of estrogen-deficient female rats with diabetes mellitus

Background

Annexin A1 (ANXA1) and the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome play important roles in bone remodeling. However, expression profiles of these factors in bone cells under diabetes mellitus (DM) and estrogen-deficient conditions are poorly understood. This study investigated the immunoexpression of ANXA1 and its formyl peptide receptor 2 (FPR2), as well as NLRP3 inflammasome mediators, during remodeling of the alveolar process in diabetic and estrogen-deficient rats.

Methods

Twenty adult female Wistar rats were divided into four groups (n = 5): Sham-operated (SHAM) and ovariectomized (OVX) rats received a vehicle solution, and SHAM and OVX rats were intraperitoneally administered 60 mg/kg/body weight (BW) of streptozotocin (STZ) to induce DM (SHAM-Di and OVX-Di groups). After 7 weeks, the rats were euthanized and their maxillae were fixed in phosphate-buffered 4% formaldehyde and embedded in paraffin. Sections were stained with hematoxylin/eosin (H&E) and picrosirius red or subjected to immunohistochemical detection of ANXA1, FPR2, NLRP3, interleukin-1β (IL-1β), and cyclooxygenase-2 (COX2).

Results

Estrogen deficiency and DM were associated with deleterious effects in bone tissue, as evidenced by a lower number of osteocytes and higher number of empty lacunae in the SHAM-Di and OVX-Di groups compared to the nondiabetic groups. Both diabetic groups showed a smaller vascular area and weaker collagen fiber birefringence intensity in alveolar bone tissue. A significantly higher number of ANXA1/FPR2-positive osteoblasts, osteocytes, and osteoclasts was accompanied by a significantly higher number of these cells immunolabeled for COX2, NLRP3, and IL-1β in the diabetic and OVX groups, especially in both estrogen-deficient and diabetic rats.

Conclusion

These results indicate a possible role for the ANXA1/FPR2 pathway as a fine-tuning/anti-inflammatory regulator to counterbalance exacerbated COX2/NLRP3/IL-1β activation in bone cells during bone remodeling under estrogen deficiency and DM.

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来源期刊
Journal of periodontology
Journal of periodontology 医学-牙科与口腔外科
CiteScore
9.10
自引率
7.00%
发文量
290
审稿时长
3-8 weeks
期刊介绍: The Journal of Periodontology publishes articles relevant to the science and practice of periodontics and related areas.
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