Helicobacter pylori (H. pylori) plays an important role in chronic atrophic gastritis (CAG). Interestingly, Shaoyao Gancao decoction (SGD), a traditional Chinese analgesic prescription, has the efficacy of relaxing spasms and relieving pain. Here, we aimed to identify whether SGD alleviates CAG and the underlying mechanism. A CAG mouse model was developed using H. pylori colonization and a high-salt diet. Histological staining was used to study the histopathological damage changes, and RT-qPCR assays the production of inflammatory responses in the gastric mucosa of mice. H. pylori and a high-salt diet induced gastric mucosal damage and apoptosis of gastric mucosal epithelial cells in mice, eliciting a significant inflammatory response. Treatment with SGD alleviated CAG-induced gastric mucosal damage, reduced apoptosis of gastric mucosal epithelial cells, and inhibited the inflammatory response. Bioinformatics was then used to construct the pharmacological network of SGD to explore its potential targets. SGD inhibited inflammatory response in mice with CAG by suppressing the expression of MAOB. Overexpression of MAOB impaired the therapeutic effect of SGD on inflammation in mice with CAG. Collectively, our findings indicated that SGD has the potential to alleviate CAG via downregulating MAOB.

Arteriosclerosis obliterans (ASO) is characterized by arterial narrowing and blockage due to atherosclerosis, influenced by endothelial dysfunction and inflammation. This research focuses on exploring the role of MAGOH-DT, a long noncoding RNA, in mediating endothelial cell dysfunction through endothelial-mesenchymal transition (EndMT) under inflammatory and hyperglycemic stimuli, aiming to uncover potential therapeutic targets for ASO. Differential expression of lncRNAs, including MAGOH-DT, was initially identified in arterial tissues from ASO patients compared to healthy controls through lncRNA microarray analysis. Validation of MAGOH-DT expression in response to tumor necrosis factor-alpha (TNF-α) and high glucose (HG) was performed in human umbilical vein endothelial cells (HUVECs) using RT-qPCR. The effects of MAGOH-DT and HNRPC knockdown on EndMT were assessed by evaluating EndMT markers and TGF-β2 protein expression with Western blot analysis. RNA-immunoprecipitation assays were used to explore the interaction between MAGOH-DT and HNRPC, focusing on their role in regulating TGF-β2 translation. In the results, MAGOH-DT expression is found to be upregulated in ASO and further induced in HUVECs under TNF-α/HG conditions, contributing to the facilitation of EndMT. Silencing MAGOH-DT or HNRPC is shown to inhibit the TNF-α/HG-induced increase in TGF-β2 protein expression, effectively attenuating EndMT processes without altering TGF-β2 mRNA levels. In conclusion, MAGOH-DT is identified as a key mediator in the process of TNF-α/HG-induced EndMT in ASO, offering a promising therapeutic target. Inhibition of MAGOH-DT presents a novel therapeutic strategy for ASO management, especially in cases complicated by diabetes mellitus. Further exploration into the therapeutic implications of MAGOH-DT modulation in ASO treatment is warranted.

Studies have found that miRNAs can participate in the progression of hypertension by affecting the function of endothelial cells and inflammatory response. This study was to investigate the clinical value of miR-320b in patients with hypertension and its potential effect on Angiotensin (Ang) II-induced endothelial cells. Real-time quantitative PCR (RT-qPCR) was used to detect the differential expression of miR-320b in all subjects, and the diagnostic value of miR-320b in hypertension was further evaluated by the receiver operating characteristic (ROC) curve. Ang II-induced human umbilical vein endothelial cells (HUVECs) were established as a model of hypertension injury. The possible downstream target gene AKT serine/threonine kinase 3 (AKT) of miR-320b was predicted through TargetScan, and the interaction between miR-320b and AKT3 was verified by luciferase reporter gene. The results showed that serum miR-320b was reduced in patients with hypertension compared with healthy people (P < 0.001). With the increase of hypertension grade, the serum miR-320b level of patients gradually decreased (P < 0.001). ROC analysis showed that miR-320b had the ability to distinguish patients from healthy people. Cell analysis proved that Ang II induced the decrease of HUVECs viability and the activation of apoptosis and inflammation, while overexpression of miR-320b inhibited Ang II-induced apoptosis and inflammation and promoted cell growth (P < 0.05). Luciferase reporter gene showed that AKT3 was the downstream target gene of miR-320b. In summary, this study suggests that miR-320b alleviates Ang II-induced apoptosis, inflammation and the inhibition of cell viability by targeting AKT3 expression, and may be involved in the pathogenesis of hypertension.

The effects of Gastrodin (GD) on cerebral ischemia stimulated researchers to investigate its possible role in the progression of arrhythmia associated with cardiac ischemia-reperfusion (IR) damage in rats. 40 Sprague-Dawley rats were divided into four groups: Sham, Model, GD 50 mg/kg, and GD 100 mg/kg. Myocardial ischemia (MI) was caused by the procedure of ligating the left coronary artery, followed by reperfusion. Heart rate (HR), mean arterial pressure (MAP), and rate pressure product (RPP) in rats were assessed before and after ischemia and reperfusion, as well as cardiac arrhythmia in experimental rats. The I/R damage was evaluated by measuring levels of Na ⁺-K⁺ATPase and Ca²⁺-Mg²⁺ATPase, Creatine Kinase-MB (CK-MB), Cardiac Troponin I (cTnI), Gap Junction α-1 (GJα-1), Phospho-GJα-1/total-GJα-1, Kir2.1, Bax, Bcl-2, and oxidative indicators. MGL’s Autodock and Vina programs were used for in silico docking studies to identify possible interactions between GJα-1 and Gastrodin. The animals in the model group expressed a substantial decrease in HR, MAP, and RPP compared to the Sham group. GD-treated rats revealed slightly higher values compared to the model group. Expression of CK-MB and cTnI was reduced, and Na⁺-K⁺ATPase and Ca²⁺-Mg²⁺ATPase expression was increased on GD pre-conditioning. Phospho-Cx43/total-Cx43 ratio and Bax expression were increased, whereas GD reduced Bcl-2 expression. In silico molecular docking studies suggested the potential binding of GD with the GJα-1 protein, thus confirming the in vivo results. GD corrected the arrhythmia in rats subjected to I/R injury by increasing Na⁺-K⁺ATPase and Ca²⁺-Mg²⁺ATPase expression, targeting GJα-1, and modulating the expression of Kir2.1.

Sleep disturbance is characterized by problems with sleep quantity and quality. However, the exact mechanisms and factors underlying sleep dissatisfaction in the general population remains unclear. This cross-sectional study collected sleep data and irritability level from individuals who visited hospitals for medical checkups or with unexplained physical symptoms using self-report questionnaires. This study included 328 individuals (157 males and 171 females). Bivariate correlation analyses revealed that irritability (ρ = 0.420; p < 0.0001), short sleep length (ρ = 0.405; p < 0.0001), difficulty falling asleep (ρ = 0.443; p < 0.0001), and nocturnal awakening (ρ = 0.528; p < 0.0001) were strongly correlated with sleep dissatisfaction. Multiple linear regression analyses among the overall individuals, following bivariate correlation analyses, indicated that stress at home (β = 0.245; p < 0.0001), irritability ( β= 0.172; p = 0.0021), difficulty falling asleep (β = 0.215; p < 0.0001), later bedtime (β = 0.140; p = 0.0331), and nocturnal awakening (β = 0.386; p < 0.0001) were independently correlated with sleep dissatisfaction, whilst short sleep length was not (β = 0.107; p = 0.1024). Further multivariable analyses revealed that difficulty falling asleep and nocturnal awakening were independently associated with each other. The obtained results were reproduced in the subgroup analyses among the 151 individuals taking medical checkups. In summary, major factors underlying sleep dissatisfaction in the general population included difficulty falling asleep and nocturnal awakening. Irritability was associated with difficulty falling asleep and sleep dissatisfaction. Carefully evaluating each of these sleep-related subscales and irritability may be beneficial in managing individuals with sleep problems.

Myeloproliferative disorders (MPDs) are rare diseases in which the bone marrow produces too many red, white, or platelets. Myeloproliferative disorders are neither acute nor leukaemia. To study ruxolitinib’s effect on MPD therapy and CD4⁺ T cell expression. In total, 66 JAK2V617F-positive MPD patients were admitted to our hospital. The patients were randomly assigned to control and research groups (each 33). Hydroxyurea pills were given to the control group and ruxolitinib to the observation group. The MPN-10 assesses 10 of the most clinically relevant symptoms, including fatigue and generates a Total Symptom Score (TSS). In addition, by comparing myelofibrosis (MF), spleen length, JAK2V617F gene expression, peripheral blood lymphocyte and T cell levels, and prognostic levels, analyze the shortcomings of each group. Post-treatment, MPN-10, MF, and spleen length diameter were reduced in both groups (P < 0.05), with the study group showing a higher reduction than the control group (P < 0.05). Compared to prior treatment, JAK2V617F gene expression was reduced in all groups after 6 months and a year of medication. The study category had a higher decrease in expression than the control group. After therapy, CD4 and CD4/CD8 levels rose, but CD8 and Treg levels decreased. The study group had increased CD4 and CD4/CD8 levels, whereas the control group had lower CD8 and Treg levels . The study group had a greater 1-year survival rate than the control group, but the control group had lower mortality and adverse event rates. In JAK2V617F-positive MPD patients, ruxolitinib reduces JAK2V617F gene expression, myelofibrosis, and therapeutic impact.

Circular RNA DLGAP4 (circ_DLGAP4) participates in the progression of ischemic stroke (IS), but whether it could regulate microglia activation to affect IS injury is unclear. This study aimed to explore the effect of circ_DLGAP4 on IS-induced microglia polarization and inflammatory cytokines, and the underlying mechanism. BV-2 cells (microglia) were transfected with circ_DLGAP4 overexpression (oeCirc), short hairpin RNA plasmid (shCirc), or corresponding negative control plasmids (oeNC and shNC). oeCirc or oeNC transfected cells were also treated with phorbol 12-myristate 13-acetate (PMA). Subsequently, BV-2 cells were treated with oxygen-glucose deprivation and reperfusion (OGD/R) to mimic IS. Circ_DLGAP4 was reduced in OGD/R-stimulated microglia versus normal microglia. Circ_DLGAP4 overexpression decreased cluster of differentiation (CD)68 and CD86, but increased CD206 and arginase-1 in OGD/R-stimulated microglia, suggesting that circ_DLGAP4 overexpression might inhibit M1 but facilitate M2 polarization of microglia. Besides, circ_DLGAP4 overexpression reduced tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, but elevated IL-10 in OGD/R-stimulated microglia, indicating that circ_DLGAP4 overexpression reduced proinflammatory cytokines but facilitated anti-inflammatory cytokines. Circ_DLGAP4 overexpression decreased p-nuclear factor kappa-B (NF-κB) and p-NF-κB inhibitor (IκB)-α in OGD/R-stimulated microglia, suggesting its inhibition of the NF-κB pathway. Notably, circ_DLGAP4 downregulation reversed the above phenomenon. PMA facilitated M1 polarization and proinflammatory cytokines but inhibited M2 polarization and anti-inflammatory cytokines in OGD/R-stimulated microglia. Interestingly, PMA attenuated the effect of circ_DLGAP4 overexpression on the above-mentioned processes in OGD/R-stimulated microglia. In conclusion, circ_DLGAP4 may attenuate IS injury by inhibiting microglia M1 polarization and proinflammatory cytokine production, which may be attributed to the inactivation of the NF-κB pathway.