Isorhamnetin has distinct anti‐inflammatory activity and inhibits cell proliferation and migration. These effects are also involved in the pathogenesis of asthma. However, the effect of isorhamnetin on bronchial epithelial cells in patients with asthma has not been examined. Cells of human bronchial epithelial cell line BEAS‐2B were cultured with isorhamnetin and tumor necrosis factor (TNF)‐α. The effects of isorhamnetin on BEAS‐2B cell viability were assessed using CCK8 assay. The EdU (5‐ethynyl‐2′‐deoxyuridine) cell proliferation assay was performed to assess cell proliferation. BEAS‐2B cell migration was measured using Transwell and wound healing assays. Real‐time PCR and enzyme‐linked immunosorbent assay were conducted to measure the expression of pro‐inflammatory cytokines. Protein expression levels were determined by western blotting. Immunofluorescence was used to detect nuclear translocation of nuclear factor kappa B (NF‐κB). We found that isorhamnetin at 20 and 40 μM reduced the proliferation of BEAS‐2B cells induced by TNF‐α. Isorhamnetin significantly decreased the expression of interleukin (IL)‐1β, IL‐6, IL‐8, and C‐X‐C motif chemokine ligand 10 in BEAS‐2B cells induced by TNF‐α. Additionally, 10 μM isorhamnetin effectively reduced cell migration induced by TNF‐α. Treatment with isorhamnetin inhibited the phosphorylation of mitogen‐activated protein kinase (MAPK) and NF‐κB pathways induced by TNF‐α. In summary, isorhamnetin inhibited the inflammation, proliferation, and migration of BEAS‐2B cells by regulating the MAPK and NF‐κB signaling pathways and is a drug candidate for asthma.

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Purpose To investigate white matter alterations in post-stroke cognitive impairment (PSCI) patients at the subacute stage employing diffusion kurtosis and tensor imaging. Methods Thirty PSCI patients at the subacute phase and 30 healthy controls (HC) underwent diffusion kurtosis imaging (DKI) scans and neuropsychological assessments. Based on the tract-based spatial statistics and atlas-based ROI analysis, fractional anisotropy (FA), mean diffusivity (MD), mean kurtosis (MK), kurtosis fractional anisotropy (KFA), axial kurtosis (AK), and radial kurtosis (RK) were compared in specific white matter fiber bundles between the groups (with family-wise error correction). Adjusting for age and gender, a partial correlation was conducted between neurocognitive assessments and DKI metrics in the PSCI group. Results In comparison with the HC, PSCI patients significantly showed decreased MK, RK, and FA and increased MD values in the genu of corpus callosum, anterior limb internal capsule, and left superior corona radiata. In addition, DKI detected more white matter region changes in MK (31/48), KFA (40/48), and RK (25/48) than DTI with FA (28/48) and MD (21/48), which primarily consisted of the right cingulum, right superior longitudinal fasciculus, and left posterior limb of internal capsule. In the left anterior limb of internal capsule, MK and RK values were significantly negatively correlated with TMT-B ( r = −0.435 and −0.414, P < 0.05), and KFA values ( r = −0.385, P < 0.05) of corpus callosum negatively associated with TMT-B. Conclusion Combing DTI, DKI, and neuropsychological tests, we found extensive damaged white matter microstructure and poor execution performance in subacute PSCI patients. DKI could detect more subtle white matter changes than DTI metrics. Our findings provide added information for exploring the mechanisms of PSCI and conducting cognitive rehabilitation in the subacute stage.

Increasing evidence suggests that immune cell infiltration is involved in primary Sjögren's syndrome (pSS), while the underlying molecular mechanisms remain elusive. Herein, this study aims to explore the key molecular mechanism in immune cell infiltration in pSS based on Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were obtained, followed by weighted gene co-expression network analysis to acquire the pSS-related module genes. Moreover, pSS-related DEGs and module genes were intersected. Additionally, the correlation between key genes and immune cell infiltration was analyzed by CIBERSORT algorithm. Furthermore, pSS mouse models were established to explore the effects of PSMC6 on immune cell infiltration and inflammatory responses in pSS. A total of 51 DEGs and 334 key module genes were involved in the occurrence of pSS. The immune cell infiltration was correlated with pSS, and PSMC6, highly expressed in pSS samples, may be the key immune gene. In vivo animal experiments demonstrated that PSMC6 was upregulated in pSS, and PSMC6 knockdown could reduce lymphocytic infiltration in salivary glands and lacrimal glands and the levels of related inflammatory factors in the pSS and increase the proportion of Treg cells. Collectively, PSMC6 could induce immune cell infiltration and inflammatory responses to promote the occurrence of pSS, providing us with a potential therapeutic target for treating pSS.