Development of a mouse model of arecoline-induced oral mucosal fibrosis

Objective: To develop a BALB/c mouse model of oral submucous fibrosis(OSF)induced by arecoline and to exhibit an accumulation of collagen and angiogenesis changes.Methods: BALB/c mice were randomly assigned to either the control(distilled water) or experimental group(arecoline)(n = 40). Eight mice from each group were sacrificed every 4 weeks since 8 weeks post treatment. Changes in histopathologic features, levels of collagen type Ⅰ and collagen type Ⅲ, and angiogenesis were measured.Results: In the 8th week, epithelium atrophy, collagen cumulation and micrangium pathologic changes in the lamina propria were observed in the oral mucosa. In the 20th week, hyaline degeneration of the connective tissues was observed on the tongue and palate mucosa. The angiogenesis and collagen type Ⅰ changed significantly as the diseases advanced(P < 0.05); however, collagen type Ⅲ was not statistically different.Conclusions: An OSF model involving mice can be rapidly induced by drinking a highdose of arecoline. OSF angiogenic changes in mice primarily decrease and collagen accumulation is mainly collagen type Ⅰ.

Research Progress in Arecoline-induced Oral Submucous Fibrosis

Areca nut is a popular fruit, but is among the most common addictions following tobacco, alcohol and caffeine globally. Areca nut chewing is the major risk factor for OSF, which is a chronic, occult, and premalignant fibrotic disease. OSF is characterized by submucosal collagen accumulation and microvascular diseases, the primary microscopic manifestations of which include damaged vascular endothelial cells, increased vascular permeability, and decreased number of microvessels. As the basic structure of microvessels, endothelial cells paly an important role in the pathogenesis and progression of OSF. Arecoline is the main component of areca nut. This review summarized the machenism of arecoline-inducing OSF by acting on endothelial cells, mainly including that arecoline can promote endothelial cells inducing tissue fibrosis by acting on the vascular endothelial cells and is accomplished via multiple aspects such as inhibiting the proliferation and facilitating the apoptosis of endothelial cells, affecting their secretion of cytokines, or promoting the transformation process of EMT.

An emerging role of arecoline on growth performance,intestinal digestion and absorption capacities and intestinal structural integrity of adult grass carp(Ctenopharyngodon idella)

Arecoline is an alkaloid with important pharmacological effects in the plant areca nut,which has been demonstrated to be an agonist of muscarinic receptors(M receptor).This study explored the influences of dietary arecoline on growth performance,intestinal digestion and absorption abilities,antioxidant capacity,and the apical junction complex(AJC)of adult grass carp(Ctenopharyngodon idella).Adult grass carp(608to 1512 g)were fed at 6 graded levels of dietary arecoline(0,0.5,1.0,1.5,2.0,and 2.5 mg/kg diet)for 9weeks.The results suggested that appropriate dietary supplementation of arecoline(1.0 mg/kg)increased growth parameters and intestinal growth in adult grass carp(P<0.05),enhanced digestion and absorption capacities(P<0.05),up-regulated muscarinic receptor 3(M3)mRNA level(P<0.05),increased the content of neuropeptide fish substance P(P<0.05),improved antioxidant capacity by activating the Keap1a/Nrf2signaling pathway(P<0.05),reduced intestinal mucosal permeability(P<0.05),and increased m RNA levels of tight junction(TJ)and adherent junction AJ-related proteins in fish by inhibiting the RhoA/ROCK signaling pathway(RhoA/ROCK/MLCK/NMII)(P<0.05).In addition,the appropriate arecoline supplementation for adult grass carp was determined to be 1.20,1.21,1.07,and 1.19 mg/kg based on percentage weight gain,lipase activity,serum diamine oxidase,and protein carbonyl,respectively.Overall,to the best of our knowledge,we investigated for the first time the effects and possible mechanisms of dietary arecoline on intestinal digestive and absorptive capacities and structural integrity in fish and evaluated the appropriate level of supplementation.

银杏外种皮对钉螺的杀灭机理

To study the toxicity of extracts of Ginkgo biloba sarcotesta to Oncomelania hupensis,snails were exposed to 40% and 80% of 24 h LC 50 of the extract of Ginkgo bilba for 24 h,choline esterase(ChE),alanine aminotransferase(ALT),alkaline phosphatase(ALP),lactate dehydrogenase(LDH),succino dehydrogenase(SDH),malic dehydrogenase(MDH)activities in cephalopodium and liver were determined by enzyme kinetic assay.Arecoline and niclosamide were used as reference molluscicides.The results showed that sarcotesta of Ginkgo biloba could inhibit ChE,ALT,ALP and MDH activities both in cephalopodium and liver;arecoline could inhibit ChE,ALP,SDH and MDH activities in cephalopodium and ChE,ALT,ALP,SDH and MDH activities in liver.Niclosamide had inhibitory effects upon ChE,ALT,ALP,SDH and MDH activities in cephalopodium,and ChE,ALT,ALP and SDH activities in liver.All three molluscicides did not inhibite LDH activity in cephalopodium and liver.These results indicate that lethal effects of extracts of sarcotesta of Ginkgo biloba are mediated via inhibition of MDH activitiy,and interference with the NADH respiratory chains.Inhibition of vital enzymic mechanisms causes snails to death.