Emodin CAS 518-82-1

Autophagy and apoptosis are important forms of degeneration and necrosis of gastrointestinal mucosal cells. It is generally believed that autophagy is a protective mechanism for the normal body, and the foreign antigens and inflammatory factors that are harmful to the body are removed through the spontaneous action of autophagy. , to ensure the balance of the internal environment of the body. It has been reported that autophagy can participate in regulating the mechanical barrier of the gastrointestinal mucosa, removing intracellular bacteria, and inhibiting inflammation. Therefore, autophagy can significantly promote the repair of the gastrointestinal mucosa. Zheng Ying et al. found that emodin can promote the division of rat small intestinal crypt epithelial cells IEC-6 cells and up-regulate the expression of autophagy-related genes Beclin-1 and LC3 in a hypoxic environment. Therefore, it is believed that emodin can promote autophagy Protective effect on gastrointestinal mucosal cells under hypoxic environment. At present, although there are few research reports on emodin promoting autophagy, existing studies have shown that emodin has anti-inflammatory, anti-aging, and free radical scavenging effects, and these effects are all involved in autophagy, so emodin protects gastric The mechanism of intestinal mucosa is definitely related to autophagy, which deserves further study.

For gastrointestinal mucosal injury, apoptosis is also one of the important mechanisms of its occurrence. Research by Zhao Hongxian and others found that diabetic rats with gastric mucosal injury would highly express the Caspase12 protein related to the apoptosis of gastric mucosal epithelial cells. In rats, ig emodin 8 g/L, 5 mL/kg, once/d, Caspase12 Down-regulation of protein expression significantly alleviated endoplasmic reticulum stress and reduced gastric mucosal damage. This study suggested that emodin can protect gastric mucosa by inhibiting the expression of Caspase12 protein, thereby inhibiting gastric mucosal apoptosis. However, some studies also believe that the mechanism of emodin’s inhibition of gastrointestinal mucosal cell apoptosis has nothing to do with the endoplasmic reticulum stress pathway. The theoretical basis and experimental basis have been established for the in-depth development of new emodin drugs based on the inhibition of gastrointestinal mucosal apoptosis. In addition, mitochondrial respiratory chain cytochrome c (cyt c) is also involved in the regulation of apoptosis. Wu Xueping’s research shows that cyt c is highly expressed in gastric mucosal epithelial cells injured in diabetic rats, so it is believed that gastric mucosal damage is related to cyt c mediated Gastric epithelial cell apoptosis is closely related. The study also administered emodin 8 g/L, 5 mL/kg, 1 time/d to model rats, and found that emodin can reduce the expression of cyt c protein in gastric mucosal cells, reduce gastric mucosal damage in rats, and relieve diabetic gastropathy. The mechanism may be that emodin can inhibit the release of cyt c from gastric mucosal epithelial cells, thereby inhibiting the activation of mitochondrial pathway and reducing the apoptosis of gastric mucosal epithelial cells. In addition, through experimental studies on rat models of severe pancreatitis, it has been found that emodin also has a protective effect on intestinal mucosal barrier damage caused by severe pancreatitis, and its mechanism is mainly through down-regulating the expression of Bax (pro-apoptotic factor) gene, thereby Inhibit the excessive apoptosis of intestinal mucosal cells, reduce the damage of intestinal mucosal barrier, and reduce the translocation of intestinal endotoxin, and finally achieve the effect of protecting the gastrointestinal mucosa.

In short, the important mechanism of emodin to protect the gastrointestinal mucosa is to promote autophagy and inhibit apoptosis, thereby alleviating the process of gastrointestinal mucosal damage and achieving the purpose of repairing the gastrointestinal mucosa.