Arecoline can be used to treat diseases including glaucoma and tapeworm infection, however, long-term administration can cause severe adverse effects, including oral submucosal fibrosis, oral cancer, hepatic injury and liver cancer. Autophagy serves a role in these injuries. The present study established a mouse model of arecoline-induced hepatic injury and investigated the role of autophagy-associated proteins in this injury. The results indicated that the expression levels of the autophagy marker protein microtubule associated protein 1 light chain 3 B (MAP1LC3B) and autophagy-promoting protein beclin 1 were elevated in the injured hepatic cells, while the expression levels of a well-known negative regulator of autophagy, mammalian target of rapamycin (mTOR), were reduced. Following treatment of the hepatic injury with glutathione, the liver function improved and liver damage was reduced effectively. Compared with the control group, the expression levels of both MAP1LC3B and beclin 1 were significantly upregulated in the glutathione-treated mice, but the expression of mTOR was significantly downregulated. It may be concluded that in the process of protecting against arecoline-induced hepatic injury, glutathione cooperates with mTOR and beclin 1 to accelerate autophagy, maintaining stable cell morphology and cellular functions.

Objectives: To investigate the feasibility of relative CT numbers to periappendiceal fat attenuation as an applicable index for estimating the severity of acute appendicitis. Methods: In total, 308 consecutive surgery-confirmed acute appendicitis patients and 243 controls with available preoperative CT were analyzed retrospectively. The radiological parameters were appendix diameter, length, and wall thickness as concurrent appendicitis signs. CT numbers of periappendiceal fat, mesenteric fat, subcutaneous fat in the anterior and posterior abdominal wall, retroperitoneal fat, gluteal subcutaneous fat and psoas major muscle were measured, as well as the relative CT numbers of periappendiceal fat compared with other locations. Results: There were 287 suppurative acute appendicitis (SAA) and 21 gangrenous or perforated acute appendicitis (GPAA) cases confirmed by pathology. The CT number of periappendiceal fat was significantly higher in patients than in controls (P＜0.01) although there was a wide overlap (−72.33 HU–117.43 HU). Significant differences in relative CT numbers were observed between the groups in gluteal subcutaneous fat (RCTgl) and psoas major muscle (RCTps) (P＜0.01). The AUCs of RCTgl and RCTps showed high accuracy to discriminate acute appendicitis from controls (AUC = 0.803, 0.761; 0.854, 0.847) and GPAA from SAA (AUC = 0.905, 0.851). Conclusions: Attenuation of periappendiceal fat on CT is related to the severity of appendicitis, and relative CT numbers (RCTgl and RCTps) could be an applicable index for severity determination. Advances in knowledge: Periappendiceal fat infiltration is related to the severity of acute appendicitis (especially relative CT number). Other clinical and CT features also need to be considered in the evaluation of inflammation.