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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.

High titer of β1-adrenoreceptor autoantibodies (β1-AA) has been reported to appear in heart failure patients. It induces sustained β1-adrenergic receptor (β1-AR) activation which leads to heart failure (HF), but the mechanism is as yet unclear. In order to investigate the mechanisms causing β1-AR non-desensitization, we studied the beating frequency of the neonatal rat cardiomyocytes (NRCMs) under different conditions (an injection of isoprenaline (ISO) for one group and β1-AA for the other) and established three dynamic models in order to best describe the true relationships shown in medical experiments; one model used a control group of healthy rats; then in HF rats one focused on conformation changes in β1-AR; the other examined interaction between β1-AR and β2-adrenergic receptors (β2-AR). Comparing the experimental data and corresponding Akaike information criterion (AIC) values, we concluded that the interaction model was the most likely mechanism. We used mathematical methods to explore the mechanism for the development of heart failure and to find potential targets for prevention and treatment. The aim of the paper was to provide a strong theoretical basis for the clinical development of personalized treatment programs. We also carried out sensitivity analysis of the initial concentration β1-AA and found that they had a noticeable effect on the fitting results.

To investigate the effect of electroacupuncture on corticotropin-releasing hormone (CRH) in the colon, spinal cord, and hypothalamus of rats with chronic visceral hypersensitivity.A rat model of chronic visceral hypersensitivity was generated according to the internationally accepted method of colorectal balloon dilatation. In the 7(th) week after the procedure, rats were randomly divided into a model group (MG), electroacupuncture group (EA), and sham electroacupuncture group (S-EA). After treatment, the abdominal withdrawal reflex (AWR) score was used to assess the behavioral response of visceral hyperalgesia. Immunohistochemistry (EnVision method), ELISA, and fluorescence quantitative PCR methods were applied to detect the expression of CRH protein and mRNA in the colon, spinal cord, and hypothalamus.The sensitivity of the rats to the colorectal distension stimulus applied at different strengths (20-80 mmHg) increased with increasing stimulus strength, resulting in increasing AWR scores in each group. Compared with NG, the AWR score of MG was significantly increased (P0.01). After conducting EA, the AWR scores of the rats were decreased compared with MG rats. The relative expression of CRH mRNA in the colon, spinal cord, and hypothalamus of MG rats was significantly increased compared with NG rats (P0.01). CRH mRNA in the colon and spinal cord of EA and S-EA rats was decreased to varying degrees (P0.05) compared with normal rats (NG). However, the decrease in EA compared with MG rats was statistically significant (P0.01). The average optical density of CRH expression in the colon of the MG rats was significantly enhanced compared with NG (P0.05), while the average optical density of CRH expression in the EA and S-EA rats was significantly decreased compared with MG rats (P0.01, P0.05, respectively). Compared with MG rats, the CRH concentration in the spinal cord of EA rats was significantly reduced (P0.01), but there was no significant change in S-EA rats (P0.05).Electroacupuncture at the Shangjuxu acupoint was able to significantly reduce the visceral hypersensitivity in rats, and regulated the expression of CRH protein and mRNA in the colon, spinal cord and hypothalamus at different levels, playing a therapeutic role in this model of irritable bowel syndrome.

It is currently accepted that the neural transduction pathways of gastrointestinal (GI) visceral pain include the peripheral and central pathways. Existing research on the neurological mechanism of electroacupuncture (EA) in the treatment of GI visceral pain has primarily been concerned with the regulation of relevant transduction pathways. The generation of pain involves a series of processes, including energy transduction of stimulatory signals in the sensory nerve endings (signal transduction), subsequent conduction in primary afferent nerve fibers of dorsal root ganglia, and transmission to spinal dorsal horn neurons, the ascending transmission of sensory signals in the central nervous system, and the processing of sensory signals in the cerebral cortex. Numerous peripheral neurotransmitters, neuropeptides, and cytokines participate in the analgesic process of EA in visceral pain. Although EA has excellent efficacy in the treatment of GI visceral pain, the pathogenesis of the disease and the analgesic mechanism of the treatment have not been elucidated. In recent years, research has examined the pathogenesis of GI visceral pain and its influencing factors and has explored the neural transduction pathways of this disease.

This study deals with the effect of moxibustion on carbonyl stress and the expression of p19ARF and p53 mRNA in livers of subacute aging rats. The SD rats were randomly divided into four groups: normal group, model group, moxibustion group, and Vit E group. Subacute aging rats were prepared with continuous high-dose intraperitoneal injection of D-galactose (D-gal). The moxibustion group received moxibustion at acupoint Shenshu (BL-23). Protein carbonyl content in livers was determined by biochemical chromatometry; p19ARF and p53 mRNA expressions were detected by fluorescence quantitative PCR. The results showed that compared with the normal group, protein carbonyl content, p19ARF, and p53 mRNA expressions were significantly higher in the model group (P < 0.01). Compared with the model group, protein carbonyl content, p19ARF, and p53 mRNA expressions were significantly lower in the moxibustion group and Vit E group (P < 0.01, P < 0.05). Our findings suggest that moxibustion at acupoint BL-23 reduced the protein carbonyl content, as well as the expression of p19ARF and p53 mRNA in livers of D-galactose-induced aging rats.