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The previous study by our group has found that miRNA‐22 can inhibit pyroptosis by targeting GSDMD and improve the memory and motor ability of mice with Alzheimer's disease (AD) mice by inhibiting inflammatory response. In recent years, stem cells and their exosomes have been reported to have good therapeutic effects on AD; therefore, we hypothesize that miRNA‐22 is likely to play a synergistic therapeutic effect. In this study, adipose‐derived mesenchymal stem cells (ADMSCs) were transfected into miRNA‐22 mimic to obtain miRNA‐22 loaded exosomes (Exo‐miRNA‐22), which was further used for the treatment and nerve repair of AD. In brief, 4‐month‐old APP/PS1 mice were assigned into the control group, Exo and Exo‐miRNA‐22 groups. After exosome transplantation, we observed changes in the motor and memory ability of mice. In addition, ELISA was used to detect the expression of inflammatory factors in cerebrospinal fluid and peripheral blood, Nissl staining was used to assess the survival of mouse nerve cells, immunofluorescence staining was used to determine the activation of microglia, and Western blot was utilized to detect the expression of pyroptosis‐related proteins. As a result, the nerve function and motor ability were significantly higher in mice in the Exo‐miRNA‐22 group than those in the control group and Exo group. Meanwhile, the survival level of nerve cells in mice was higher in the Exo‐miRNA‐22 group, and the expression of inflammatory factors was lower than that of the Exo group, indicating Exo‐miRNA‐22 could significantly suppress neuroinflammation. In vitro culture of PC12 cells, Aβ25‐35‐induced cell damage, detection of PC12 apoptotic level, the release of inflammatory factors and the expression of pyroptosis‐related proteins showed that Exo‐miRNA‐22 could inhibit PC12 apoptosis and significantly decrease the release of inflammatory factors. In this study, we found that miRNA‐22‐loaded ADMSC‐derived exosomes could decrease the release of inflammatory factors by inhibiting pyroptosis, thereby playing a synergetic therapeutic role with exosomes on AD, which is of great significance in AD research.

Our previous research has found that miRNA‐22 can inhibit the occurrence of pyroptosis by targeting GSDMD and decrease the production and release of inflammatory factors. In consideration of the therapeutic effects of mesenchymal stem cells (MSCs), MSCs‐EV were loaded with miRNA‐22 (EV‐miRNA‐22) to investigate the inhibitory effect of EV‐miRNA‐22 on the inflammatory response in SCI in rats in this study. LPS/Nigericin (LPS/NG) was used to induce pyroptosis in rat microglia in vitro. Propidium iodide (PI) staining was performed to observe cell permeability, lactate dehydrogenase (LDH) release assay was adopted to detect cytotoxicity, flow cytometry was conducted to detect pyroptosis level, immunofluorescence (IF) staining was utilized to observe the expression level of GSDMD (a key protein of pyroptosis), Western blot was performed to detect the expression of key proteins. For animal experiments, the T10 spinal cord of rats was clamped by aneurysm clip to construct the SCI model. BBB score, somatosensory evoked potential (SEP) and motor evoked potential (MEP) were performed to detect nerve function. HE staining and Nissl staining were used to detect spinal cord histopathology and nerve cell damage. EV‐miRNA‐22 could inhibit the occurrence of pyroptosis in microglia, suppress the cell membrane pore opening, and inhibit the release of inflammatory factors and the expression of GSDMD. In addition, EV‐miRNA‐22 showed higher pyroptosis‐inhibiting ability than EV. Consequently, EV‐miRNA‐22 could inhibit the nerve function injury after SCI in rats, inhibit the level of inflammatory factors in the tissue and the activation of microglia. In this study, we found that miRNA‐22‐loaded MSCs‐EV (EV‐miRNA‐22) could cooperate with EV to inhibit inflammatory response and nerve function repair after SCI.

Background Currently, acute myocardial infarction (AMI) represents a serious cardiovascular disease with high morbidity and mortality. Therefore, this study aimed to systematically evaluate the roles of miRNA‐499 and miRNA‐22 as potential biomarkers for AMI. Methods According to the inclusion and exclusion criteria, we measured circulating levels of miRNAs in 50 AMI patients and 50 non‐MI populations. The expression levels of plasma miRNA‐499 and miRNA‐22 were analyzed by real‐time fluorescent quantitative polymerase chain reaction (qRT‐PCR). A statistical analysis of clinical data of AMI patients was conducted by 90‐day follow‐up. Results Real‐time PCR analysis showed that the relative expression level of miRNA‐499 increased gradually among the three groups (P < .05). However, the expression of miRNA‐22 showed a downward trend (P < .05). According to logistic analysis, the relative levels of miRNA‐499 and miRNA‐22 were important predictors of AMI. When the miRNA‐499 and miRNA‐22 levels were 0.377 and 0.946 separately, the diagnostic value of miRNA‐499 and miRNA‐22 for AMI was 86.00% and 86.00% for sensitivity, and 98.00% and 94.00% for specificity, respectively. In addition, compared to the baseline GRACE scoring system, the combination of miRNA‐499, miRNA‐22, and GRACE scores had a stronger discriminating power for MACE occurrence, with a sensitivity of 100.00% and a specificity of 79.40%. Conclusions The results showed that plasma miRNA‐499 and miRNA‐22 were more sensitive and specific for the diagnosis of AMI, suggesting that they can be used as potential biomarkers for clinical diagnosis of AMI.