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2型糖尿病大鼠腮腺和颌下腺的组织病理学损伤及分泌功能障碍导致基础和刺激唾液参数降低。

Decreased basal and stimulated salivary parameters by histopathological lesions and secretory dysfunction of parotid and submandibular glands in rats with type 2 diabetes.

作者信息

Chen Si-Yu, Wang Ying, Zhang Chun-Lei, Yang Ze-Min

机构信息

Department of Biochemistry and Molecular Biology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, P.R. China.

Department of Stomatology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China.

出版信息

Exp Ther Med. 2020 Apr;19(4):2707-2719. doi: 10.3892/etm.2020.8505. Epub 2020 Feb 10.

Abstract

Patients with type 2 diabetes mellitus (T2DM) present with dry mouth, polydipsia and taste impairment due to salivary secretion disorder. However, the underlying functional mechanism of T2DM remains unknown. The present study found that T2DM rats had significantly lower salivary flow rate and salivary alpha amylase activity, and attenuated salivary secretion responses to acid stimulation compared with control rats. Histopathological observation found that T2DM rats had inflammatory cell infiltration with increased expressions of IL-6 and TNF-α, oxidative stress, including decreased total superoxide dismutase activity and increased malondialdehyde content, and decreased expressions of β1 adrenergic receptor, cholinergic receptor, aquaporin-5 and protein kinase A in salivary glands, in particular the parotid gland. These results indicated that parotid gland impairment was more severe compared with submandibular gland impairment. Reduced salivary secretion may be associated with histopathological lesions and decreased regulation in secretory pathways in salivary glands.

摘要

2型糖尿病(T2DM)患者由于唾液分泌紊乱而出现口干、多饮和味觉障碍。然而,T2DM的潜在功能机制仍不清楚。本研究发现,与对照大鼠相比,T2DM大鼠的唾液流速和唾液α淀粉酶活性显著降低,对酸刺激的唾液分泌反应减弱。组织病理学观察发现,T2DM大鼠存在炎性细胞浸润,IL-6和TNF-α表达增加,存在氧化应激,包括总超氧化物歧化酶活性降低和丙二醛含量增加,唾液腺尤其是腮腺中β1肾上腺素能受体、胆碱能受体、水通道蛋白-5和蛋白激酶A的表达降低。这些结果表明,与下颌下腺损伤相比,腮腺损伤更严重。唾液分泌减少可能与组织病理学病变以及唾液腺分泌途径调节降低有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e9e9/7086285/3ef1f77d7cdc/etm-19-04-2707-g00.jpg

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