Antiulcerogenic Activity of Li-Zhong Decoction on Duodenal Ulcers Induced by Indomethacin in Rats: Involvement of TLR-2/MyD88 Signaling Pathway

Houpan Song; Meiyan Zeng; Xiaojuan Chen; Xinyi Chen; Jun Peng; Ye Lin; Rong Yu; Xiong Cai; Qinghua Peng

doi:10.1155/2020/6538156

Antiulcerogenic Activity of Li-Zhong Decoction on Duodenal Ulcers Induced by Indomethacin in Rats: Involvement of TLR-2/MyD88 Signaling Pathway

Evid Based Complement Alternat Med. 2020 Jan 21:2020:6538156. doi: 10.1155/2020/6538156. eCollection 2020.

Authors

Houpan Song^{1

2}, Meiyan Zeng², Xiaojuan Chen^{1

2}, Xinyi Chen^{1

2}, Jun Peng³, Ye Lin^{1

2}, Rong Yu², Xiong Cai⁴, Qinghua Peng¹

Affiliations

¹ Institute of Traditional Chinese Medicine Diagnostics, Hunan University of Chinese Medicine, Changsha, Hunan, China.
² College of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, China.
³ Department of Ophthalmology, the First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China.
⁴ Institute of Innovation and Applied Research, Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, China.

Abstract

Background: Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) often causes small intestinal ulcers in patients, but few effective drugs are currently available to manage such serious adverse events of NSAIDs. Li-Zhong decoction (LZD), a well-known traditional Chinese medicine (TCM) formula, is commonly prescribed for treatment of gastrointestinal diseases. The present study aimed to investigate the anti-ulcerogenic activity of LZD on indomethacin- (IND-) induced duodenal ulcer in rats. Mechanistic studies of action of LZD were focused on involvement of TLR-2/MyD88 signaling pathway.

Methods: Fifty male Sprague-Dawley (SD) rats were randomly and evenly divided into five groups: normal control, ulcer control (IND, 25 mg/kg), IND + esomeprazole (ESO, 4.17 mg/kg), and IND + low and high doses of LZD (3.75 and 7.50 g/kg). Macroscopic and histopathological examinations were performed for evaluation of ulcer index (UI), curative index (CI), and microscopic score (MS). Levels of duodenal inflammatory biomarkers and cytoprotective mediators including interleukin-4 (IL-4), IL-10, tumor necrosis factor-α (TNF-α (TNF.

Results: Gross and microscopic examinations of the IND-treated rats revealed severe duodenal hemorrhagic necrosis, inflammatory infiltration, villus destruction, and crypt abscess, while LZD-treated rats manifested these pathological events to a markedly lesser degree. LZD significantly decreased UI and MS, increased CI, preserved the integrity of the villus and crypt, and normalized the tissue architecture of the duodenum of rats. The elevated TNF-α (TNF.

Conclusions: Our data demonstrate that LZD protects the duodenal mucosa from IND-caused lesions, which is at least partially attributable to the interaction of its potential cytoprotective and anti-inflammatory mechanisms together with enhancement of the mucosal immunity through TLR-2/MyD88 signaling pathway.