Integration of bioinformatics analysis, molecular docking and animal experiments to study the therapeutic mechanisms of berberine against allergic rhinitis.

Allergic rhinitis is a prevalent inflammatory condition that impacts individuals of all age groups. Despite reports indicating the potential of berberine in alleviating allergic rhinitis symptoms, the specific molecular mechanisms and therapeutic targets of berberine remain unclear. This research aims to explore the pharmacological mechanism of berberine in the treatment of allergic rhinitis through bioinformatic analyses and experimental validation. The research utilized public databases to identify potential targets of berberine. Furthermore, differentially expressed genes (DEGs) related to allergic rhinitis were pinpointed from the GSE52804 dataset. Through bioinformatics techniques, the primary targets were discovered and key KEGG and GO-BP pathways were established. To confirm the therapeutic mechanisms of berberine on allergic rhinitis, an OVA-induced allergic rhinitis model was developed using guinea pigs. We identified 32 key genes responsible for the effectiveness of berberine in treating allergic rhinitis. In addition, five central genes (Alb, Il6, Tlr4, Ptas2, and Il1b) were pinpointed. Further examination using KEGG and GO-BP pathways revealed that the main targets were primarily involved in pathways such as NF-kappa B, IL-17, TNF, and inflammatory response. Molecular docking analysis demonstrated that berberine exhibited strong affinity towards these five key targets. Furthermore, the expression levels of IL-6, TLR4, PTGS2, and IL-1ß were significantly upregulated in the model group but downregulated following berberine treatment. This research has revealed the mechanism through which berberine combats allergic rhinitis and has identified its potential to regulate pathways linked to inflammation. These discoveries provide valuable insights for the development of novel medications for the treatment of allergic rhinitis.

Lowered circulating apelin is significantly associated with an increased risk for hypertension: A meta-analysis.

BACKGROUND AND OBJECTIVE: Apelin is a bioactive peptide manifesting a potent vasodilatory property. In this meta-analysis, we aimed to investigate for the first time whether circulating apelin differed significantly between hypertensive patients and normotensive controls. METHODS: Both PubMed and Embase were searched for eligible articles. Eligibility evaluation and data collection were done independently by two investigators. Weighted mean difference (WMD) with 95% confidence interval (CI) was calculated under random-effects model by STATA. RESULTS: Ten studies were synthesized finally, including 1610 patients and 1105 controls. Overall analysis revealed that circulating apelin was significantly lowered in patients than in controls (WMD = -39.85 pg/mL, 95% CI: -65.56 to -14.15; P = 0.002), with significant heterogeneity (I2 = 89.4%). By race, patients had lower circulating apelin than controls in Caucasian populations (WMD = -79.82 pg/mL, 95% CI: -105.80 to -53.85; P < 0.001), without heterogeneity (I2=0.0%), while no significance was observed in Chinese and African-Americans. Further grouping studies by source of controls found a significant reduction in circulating apelin in studies with hospital-based controls (WMD = -96.28 pg/mL, 95% CI: -129.67 to -62.88; P < 0.001) (I2 = 49.4%), but not in studies with population-based controls. CONCLUSIONS: Via a meta-analysis of 10 studies and on 2715 subjects, our findings demonstrated that lowered circulating apelin was significantly associated with an increased risk for hypertension, especially in Caucasian populations.

A meta-analytical comparison of atenolol with angiotensin-converting enzyme inhibitors on arterial stiffness, peripheral blood pressure and heart rate in hypertensive patients.

OBJECTIVES: This meta-analysis of randomized parallel controlled trials was designed to compare the efficacy of atenolol with angiotensin-converting enzyme inhibitors (ACEIs) in changing pulse wave velocity (PWV), peripheral blood pressure and heart rate (HR) among patients with essential hypertension. METHODS: This study was conducted according to the PRISMA guideline. Data collection was independently completed by two investigators. Statistical analyses were completed by Stata software (v12.0). RESULTS: Eight clinical trials were meta-analyzed in this study. Overall changes in PWV (weighted mean difference or WMD = 0.068, 95% confidence interval or CI: -0.487 to -0.623, P = 0.811) and peripheral systolic blood pressure (PSBP) (WMD = -1.281 mmHg, 95% CI: -6.936 to 4.375, P = 0.657) did not differ significantly between atenolol and ACEIs treatment. Relative to ACEIs, atenolol had a more favorable impact on peripheral diastolic blood pressure (PDBP) (WMD = -1.912 mmHg, 95% CI: -3.732 to -0.091, P = 0.040) and HR (WMD = -9.23 bpm, 95% CI: -12.53 to -5.93, P < 0.001). In stratified analyses, particularly by follow-up period, atenolol was observed to be superior over ACEIs within early 3-month treatment in PSBP (WMD = -4.097 mmHg, 95% CI: -6.589 to -1.605, P = 0.001), PDBP (WMD = -6.802 mmHg, 95% CI: -8.517 to -5.087, P < 0.001) and HR (WMD = -14.242 bpm, 95% CI: -16.427 to -12.058, P = 0.028), without heterogeneity (I2 = 0.0%). There were low probabilities of publication bias for all comparisons. CONCLUSIONS: Our findings demonstrate that atenolol and ACEIs were equally effective in reducing PWV and PSBP, while atenolol was superior over ACEIs in improving PDBP and HR, especially within short-term treatment.

[Effects of ampelopsin on invasion and metastasis of B16 mouse melanoma in vivo and in vitro].

OBJECTIVE: To investigate the effects of ampelopsin on B16 melanoma's invasion and metastasis in vivo and in vitro. METHOD: B16 mouse melanoma cells were injected into C57BL/6 mouse via tail lateral vein, which subsequently colonized into the animal lungs to form an experimental pulmonary metastasis of tumor cell. The ampelopsin was administered at 3 dosages by intraperitoneal injection daily for 18 days from the day before the cells injection. The B16 mouse melanoma cells were exposed to ampelopsin for 3 days. The effects of ampelopsin on invasion, migration and adhesion of B16 melanoma cells were evaluated with Transwell chambers or attachment with polycarbonate filters and reconstituted basement membrane (Matrigel). RESULT: The number of metastases in the animals that were given ampelopsin 150, 200, and 250 mg x kg(-1) x d(-1) was significantly reduced as compared to the vehicle control (P<0.05), and the inhibition rates were 30.97%, 40.58%, and 61.16%, respectively. The ability of the ampelopsin treated B16 cells to invade the reconstituted basement membrane was decreased significantly (P<0.01), and the inhibition rates were 36.06%, 59.58%, and 79.09% at 20 micromol x L(-1), 40 micromol x L(-1) and 80 micromol x L(-1) concentration, respectively. Ampelopsin could also inhibit B16 cells migration through PVPF in the Transwell chambers, and the inhibition rates were 51.59%, 56.51%, and 66.75% at 20 micromol x L(-1), 40 micromol x L(-1) and 80 micromol x L(-1), respectively (P<0.01). The ability of adhesion of the B16 cells by ampelopsin treated cells on fibronectin, laminin, or Matrigel was decreased significantly. CONCLUSION: Ampelopsin has anti-invasive and anti-metastatic effects on B16 melanoma.