Accumulating evidence demonstrates that microRNA- (miR-) mediated posttranscriptional regulation plays an important role in autophagy in inflammatory bowel disease (IBD), a disease that is difficult to manage clinically because of the associated chronic recurrent nonspecific inflammation. Research indicates that microRNAs regulate autophagy via different pathways, playing an important role in the IBD process and providing a new perspective for IBD research. Related studies have shown that miR-142-3p, miR-320, miR-192, and miR-122 target NOD2, an IBD-relevant autophagy gene, to modulate autophagy in IBD. miR-142-3p, miR-93, miR-106B, miR-30C, miR-130a, miR-346, and miR-20a regulate autophagy by targeting ATG16L1 through several different pathways. miR-196 can downregulate IRGM and suppress autophagy by inhibiting the accumulation of LC3II. During the endoplasmic reticulum stress response, miR-665, miR-375, and miR-150 modulate autophagy by regulating the unfolded protein response, which may play an important role in IBD intestinal fibrosis. Regarding autophagy-related pathways, miR-146b, miR-221-5p, miR-132, miR-223, miR-155, and miR-21 regulate NF-κB or mTOR signaling to induce or inhibit autophagy in intestinal cells by releasing anti- or proinflammatory factors, respectively.

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Allergic asthma is associated with T helper (Th) 2 cell-biased immune responses and characterized by the airway hyperresponsiveness (AHR). Studies have shown that the acupoint catgut-embedding therapy (ACE) has a therapeutic effect on allergic asthma. However, the relevant mechanism is poorly understood. In present study, female BALB/c mice were sensitized and challenged with ovalbumin (OVA) to establish a model of allergic asthma. AHR was evaluated by using airway resistance ( R L ) and lung dynamic compliance (Cdyn). Airway inflammation and mucus hypersecretion were observed by HE and PAS staining. Inflammatory cells were counted, and related cytokines in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Pulmonary group 2 innate lymphoid cell (ILC2s) proportions were analyzed by flow cytometry. The expression of nuclear factor κB (NF-κB) and cyclooxygenase-2 (COX-2) was detected by immunostaining. Our results showed that OVA induction resulted in a significant increase in R L , accompanied by a significant decrease in Cdyn. The levels of interleukin- (IL-) 4, IL-13, OVA-specific IgE in BALF, and the percentage of ILC2 in the lungs were markedly increased accompanied by a significant decreased in interferon-γ (IFN-γ). Furthermore, the expressions of p-NF-κB p65 and COX-2 in airways were significantly upregulated. After ACE treatment, the indicators above were significantly reversed. In conclusion, ACE treatment inhibited the secretion of Th2 cytokines and the proliferation of ILC2s in the lungs, thereby dampening the inflammatory activity in allergic asthma. The underlying mechanism might be related to the inhibition of NF-κB/COX-2 pathway.