An exosome (30–150 nm size) is a cell-derived vesicle. Exosome-induced regulation in inflammatory bowel disease (IBD) is becoming increasingly popular due to their potential functions of exosomal pathways. Exosomes, which are involved in the regulation of IBD, can be released from various cell types, or found in many physiological fluids, and plants. The specific functions of exosomes in IBD primarily depend on the internal functional components, including RNAs, proteins, and other substances. However, exosome-induced transport mechanisms involving cell-cell communications or cell-environment interactions are also very important. Recent studies have revealed that exosome crosstalk mechanisms may influence major IBD-related pathways, such as immune responses, barrier functions, and intestinal flora. This review highlights the advancements in the biology of exosome secretions and their regulation in IBD. The functional roles of exosomal components, including nucleic acids, proteins, and some other components, are the main focus of this review. More animal and clinical research is needed to study the functions of exosomes on IBD. Designing new drug dosage form using exosome-like-structure may provide new insights into IBD treatment. This review suggests a potential significance for exosomes in IBD diagnosis and treatment.

Myosin light chain kinase (MLCK) induces contraction of the perijunctional apical actomyosin ring in response to phosphorylation of the myosin light chain. Abnormal expression of MLCK has been observed in respiratory diseases, pancreatitis, cardiovascular diseases, cancer, and inflammatory bowel disease (IBD). The signaling pathways involved in MLCK activation and triggering of endothelial barrier dysfunction are discussed in this review. The pharmacological effects of regulating MLCK expression by inhibitors such as ML-9, ML-7, microbial products, naturally occurring products, and microRNAs are also discussed. The influence of MLCK in inflammatory diseases starts with endothelial barrier dysfunction. The effectiveness of anti-MLCK treatment may depend on alleviation of that primary pathological mechanism. This review summarizes evidence for the potential benefits of anti-MLCK agents in the treatment of inflammatory disease and the importance of avoiding treatment-related side effects, as MLCK is widely expressed in many different tissues.

Parkinson’s disease (PD) is the second most common neurodegenerative disease which significantly influences the life quality of patients. The protein α-synuclein plays an important driving role in PD occurrence and development. Braak’s hypothesis suggests that α-synuclein is produced in intestine, and then spreads into the central nervous system through the vagus nerve. The abnormal expression of α-synuclein has been found in inflammatory bowel disease (IBD). Intestinal inflammation and intestinal dysbiosis have been involved in the occurrence and development of PD. The present review aimed to summarize recent advancements in studies focusing on intestinal inflammation and PD, especially the mechanisms through which link intestinal inflammation and PD. The intestinal dysfunctions such as constipation have been introduced as non-motor manifestations of PD. The possible linkages between IBD and PD, including genetic overlaps, inflammatory responses, intestinal permeability, and intestinal dysbiosis, are mainly discussed. Although it is not confirmed whether PD starts from intestine, intestinal dysfunction may affect intestinal microenvironment to influence central nervous system, including the α-synuclein pathologies and systematic inflammation. It is expected to develop some new strategies in the diagnosis and treatment of PD from the aspect of intestine. It may also become an exciting direction to find better ways to regulate the composition of gut microorganism to treat PD.

Inhibition of ferroptosis in intestinal epithelial cells ameliorates clinical symptoms and improves endoscopic presentations in inflammatory bowel disease (IBD).