Effects of Huanglian Jiedu Decoration in Rat Gingivitis.

Ya Geng,Defeng Li,Baolin Bian,Hongjun Yang,Haiyu Zhao,Yi Zhang,Hongjie Wang,Fangbo Zhang

doi:10.1155/2018/8249013

Abstract

Gingivitis is an inflammatory disease that affects gingival tissues through a microbe-immune interaction. Huanglian Jiedu decoction (HLJD) is used traditionally for clearing and detoxifying in China, which had been reported to possess many pharmacological effects. Rat gingival inflammation model was established by lipopolysaccharide (LPS) injection for 3 consecutive days, and HLJD was given by gavage before LPS injection. After 3 days rats were sacrificed and tissue samples were evaluated. Serum cytokine levels such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunoabsorbent assay (ELISA). Oxidative stress related molecules such as total antioxidant capacity (T-AOC), malondialdehyde (MDA), and reactive oxygen species (ROS) were determined. Expression of AMP-activated protein kinase (AMPK) and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathway were inspected by western blotting. Histological changes of gingival tissues were tested with hematoxylin-eosin (HE) staining. HLJD significantly decreased serum levels of IL-6 and TNF-α, suppressed generation of MDA and ROS, and enhanced T-AOC creation. Moreover, HLJD inhibited expressions of AMPK and ERK1/2. The inflammation severity of gingival tissue by HE staining was severe in model group but relieved in HLJD group obviously. HLJD exhibited protective effects against gingival damage through suppressing inflammation reaction and elevating antioxidation power.

Highlights

Gingivitis is the most common form of periodontal disease affecting 50% to 90% of the adults worldwide [1]
Lipopolysaccharide (LPS) is an endotoxin generated by gram-negative bacteria, which influences lipoxygenase and cyclooxygenase inflammatory pathways and results in production of proinflammatory cytokines such as prostaglandin (PG), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) [5]
Serum inflammatory cytokines including IL-6 and TNF-α were analyzed by enzyme-linked immunoabsorbent assay (ELISA) test

Summary

Introduction

Gingivitis is the most common form of periodontal disease affecting 50% to 90% of the adults worldwide [1]. Gingivitis is a chronic inflammatory reaction caused by mainly gramnegative bacteria It is mediated by upregulation of synthesis and release of various proinflammatory factors leading to excessive injury [2, 3]. Lipopolysaccharide (LPS) is an endotoxin generated by gram-negative bacteria, which influences lipoxygenase and cyclooxygenase inflammatory pathways and results in production of proinflammatory cytokines such as prostaglandin (PG), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) [5]. These cytokines destroy periodontal tissue and alveolar bone, eventually leading to tooth loss. In our research experimental animal model was established by LPS injection in rat gingivitis as reported [7, 8]

Methods

Results

Conclusion