Sepsis is an organ dysfunction that endangers a patient's life caused by an imbalanced infection response, and is a clinically critical illness. Despite a deep understanding of the pathogenesis of sepsis, there has been no significant improvement in sepsis mortality during clinical treatment at home and abroad. In recent years, the role of autophagy in the pathogenesis of sepsis has become a new research point in the field of medical research. Autophagy may protect the body by removing pathogenic microorganisms, neutralizing microbial toxins, and regulating cytokine release in sepsis. Studies have shown that autophagy plays a role in heart and lung organ dysfunction and inflammatory immune response in sepsis. Studies have also shown that hydrogen sulphide (H 2S) can activate autophagy through multiple signaling pathways, such as adenylate-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR), phosphoinositide 3 kinase/Akt/mTOR (PI3K/Akt/mTOR), liver kinase B1/STE20 related adapter protein/mouse protein 25 (LKB1/STRAD/MO25) and microRNA-30c (miR-30c), etc. signaling pathways. This article reviewed the effects of H 2S on autophagy-related genes Beclin-1 and microtubule-associated protein light 3 chain (LC3) on intestinal function of sepsis in order to explore the H 2S-mediated autophagy gene expression in pus. The protective role of autophagy gene for intestinal dysfunction provides a new strategy for the treatment of sepsis in the future.

Sepsis is one of the main causes of death in critically ill patients. The intestinal tract is not only the organ easily involved in sepsis, but also the initial organ in the progression of sepsis, so the improvement of intestinal barrier function is the key of the treatment of sepsis. In recent years, it has been found that autophagy is involved in the pathological process of sepsis, maintaining mitochondrial function by clearing damaged organelles, inhibiting inflammation, oxidative stress and apoptosis, regulating immunity, maintaining intestinal homeostasis, and improving the condition and prognosis of sepsis. It is an effective target for the treatment of sepsis. As a new type of medical gas signal molecule, hydrogen sulfide (H 2S) can regulate autophagy by regulating multiple signal pathways, which has become a new target in the treatment of sepsis. This article reviews the signal pathway regulation mechanism of H 2S regulating autophagy in septic intestinal dysfunction.

Melatonin is an indoleamine secreted by the pineal gland and plays a key role in a variety of physiological activities, including the regulation of circadian rhythm, immune response, oxidative process and apoptosis. In recent years, the anti-tumor properties of melatonin have attracted more and more attention. A large number of studies have found that melatonin plays a protective role in the early process of acute pancreatitis and can inhibit the production of pancreatic adenocarcinoma cells through apoptosis; moreover, it can regulate the synthesis and secretion of pancreatic endocrine hormones through autophagy and affect the development of pancreatic endocrine tumors. Therefore, melatonin may affect the development of pancreatic disease, but the mechanism of its action on pancreatic diseases has not been fully understood. This paper reviews the research progress of melatonin and pancreatic diseases in recent years, analyzes the role of melatonin in pancreatic diseases and the therapeutic effect of melatonin combined with chemotherapy drugs on pancreatic cancer.

The Hedgehog (HH) signaling pathway plays important roles in gastrointestinal carcinogenesis and the gastrointestinal tumor microenvironment (TME). Aberrant HH signaling activation may accelerate the growth of gastrointestinal tumors and lead to tumor immune tolerance and drug resistance. The interaction between HH signaling and the TME is intimately involved in these processes, for example, tumor growth, tumor immune tolerance, inflammation, and drug resistance. Evidence indicates that inflammatory factors in the TME, such as interleukin 6 (IL-6) and interferon-