Abstract
Ethanol-induced gastric mucosal injury is a common gastrointestinal disorder. Polysaccharides separated from herbs have been shown to be effective for ethanol-induced gastric mucosal injury, but whether the polysaccharides from Dendrobium officinale Kimura & Migo leaves (LDOP-1) protected mucosa from ethanol-induced injury remains unknown. Thus, the present study carried out gastric mucosal protection and the mechanism of LDOP-1 in vivo and vitro. The chemical composition of LDOP-1 was a heteropolysaccharide comprising mannose, galacturonic acid, glucose, galactose, and arabinose at a molar ratio of 2.0:1.1:0.7:0.5:0.4. Pharmacological results showed that LDOP-1 significantly reduced gastric mucosal injury score and pathological injury, improved antioxidant capacity, reduced the level of reactive oxygen species, and reversed the apoptosis of GES-1 in vivo and vitro. Research showed that LDOP-1 pretreatment upregulated the expression level of p-AMPK, LC3β, HO-1, and Beclin-1; downregulated the expression level of p-mTOR and p62; and reversed the expression level of caspase3, Bax, and Bcl-2. This study was the first to demonstrate that LDOP-1 could protect against ethanol-induced gastric mucosal injury via the AMPK/mTOR signaling pathway in vitro and vivo.
Highlights
Ethanol-induced gastric mucosal injury is a common gastrointestinal disorder that is characterized by hemorrhage, erosion, ulcers, and loss of the gastric mucosa (Matsuda et al, 2002; Senol et al, 2011)
The pretreatment with low- or high-dose LDOP-1 and the OME group could significantly mitigate the mucosal injury area induced by ethanol and decrease the ulcer index in rat gastric mucosa compared with the model group
We found that Dendrobium officinale Kimura & Migo leaves (LDOP-1) reversed the Bax/Bcl2 ratio and the levels of caspase 3 in vivo and vitro, which indicated that LDOP-1 might be related to the decrease of gastric mucosal cell apoptosis
Summary
Ethanol-induced gastric mucosal injury is a common gastrointestinal disorder that is characterized by hemorrhage, erosion, ulcers, and loss of the gastric mucosa (Matsuda et al, 2002; Senol et al, 2011). Polysaccharides Protected Ethanol-Induced Mucosal Injury cell apoptosis, inflammatory reaction, and oxidative stress in gastric tissue (Jiang et al, 2015). Some reports have found that the generation of ROS could activate caspase and downregulate the ratio of Bcl-2 and Bax, which leads to cell apoptosis (Fulda et al, 1997; Wang et al, 2017). This finding indicates that the antioxidant system plays an important role in protecting the gastrointestinal mucosal layer against gastric damage (Shin et al, 2013)
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