Prostaglandins & other lipid mediators最新文献

The nervous system interacts with the immune system through a variety of cellular regulators, signaling pathways, and molecular mechanisms. Disruptions in these interactions lead to the development of multiple neurological diseases. Recent studies have identified that specialized pro-resolving mediators (SPMs) play a regulatory role in the neuroimmune system. This study reviews recent research on the function of SPMs in the inflammatory process and their association with the nervous system. The review aims to provide new perspectives for studying the pathogenesis of neurological diseases and identify novel targets for clinical therapy.

Several interventional studies have revealed the beneficial impact of curcumin supplementation on blood pressure and endothelial function, but the findings are conflicting. Therefore, this study was conducted to investigate the effects of curcumin supplementation on blood pressure and endothelial function. A meta-analyses of randomized clinical trials were performed by searching PubMed, Embase, Scopus, and Web of Science were searched up to March 31, 2024. Random effects models were used to calculate weighted mean differences (WMD). Pooled estimates of 10 studies revealed that curcumin decreased diastolic blood pressure (DBP) [WMD = −0.94, 95 % CI: −1.59, −0.30; p = 0.004], pulse wave velocity (PWV) [WMD = −45.60, 95 % CI: −88.16, −3.04; p = 0.03, I² = 0.0 %, p = 0.59], and vascular cell adhesion molecule-1 (VCAM-1) [WMD = −39.19; 95 % CI: −66.15, −12.23, p =0.004; I²=73.0 %, p = 0.005] significantly, and increased flow-mediated dilation (FMD) [WMD = 1.64, 95 % CI: 1.06, 2.22; p < 0.001, I² = 0.0 %, p = 0.61. However, curcumin did not significantly change systolic blood pressure (SBP) [WMD = −0.64, 95 % CI: −1.96, 0.67; p =0.34, I² = 83.5 %, p <0.001], and Intercellular Adhesion Molecule 1 (ICAM1) [WMD = −17.05; 95 % CI: −80.79, 46.70, p =0.601; I²=94.1 %, p < 0.001]. These results suggest that curcumin has a beneficial effect on DBP, PWV, VCAM-1 and FMD levels and may be an effective adjunctive therapy for improving blood pressure and endothelial function.

Several studies have evaluated the effects of resveratrol supplementation on lipid profile parameters in humans and have demonstrated varying results. We systematically evaluated the literature and performed an umbrella meta-analysis of the effects of resveratrol supplementation on lipid profile. A comprehensive literature search was conducted in the following databases; PubMed, Embase, Scopus, and Web of Science for studies published up to November 2023. According to the standardized mean difference (SMD) analysis, resveratrol supplementation was effective in reducing serum triglyceride (TG) (SMD = −0.14 mg/dl, 95 % CI: −0.24, −0.03; p = 0.001), total cholesterol (TC) (SMD = −0.20, 95 % CI: −0.31, −0.08; p= 0.001), but not high-density lipoprotein cholesterol (HDL-c) (SMD = 0.00, 95 % CI: −0.04, 0.05; p =0.92), and low-density lipoprotein-cholesterol (LDL-c) (SMD = −0.16 mg/dl, 95 % CI: −0.40, 0.07; p =0.17). In the weighted mean difference analysis, resveratrol did not significantly decrease lipid profile parameters. Resveratrol supplementation reduces TC and TG (based on SMD analysis), but it does not significantly affect other indices. However, these significant decreases are not clinically important. Therefore, resveratrol only can be considered as an adjunctive therapeutic approach in managing dyslipidemia.

Background & aims

Taking into account the anti-inflammatory and antioxidant properties of omega-3 fatty acids and the evidence indicating the role of chronic inflammation and oxidative stress in the pathophysiology diabetes, this study aimed to determine the effect of ω−3 fatty acids on oxidative stress and inflammatory markers in Type 2 diabetes mellitus (T2DM) patients.

Methods

A systematic search up to July 30, 2023 was completed in Scopus, PubMed, Web of Science, and Embase databases, to identify eligible RCTs. Heterogeneity tests of the selected studies were performed using the I². Random effects models were assessed and pooled data were determined as standardized mean differences (SMD) with a 95 % CI.

Results

The meta-analysis of 23 trials, involving 1523 patients, demonstrated a significant decrease in TNF-α (SMD: −1.62, 95 % CI: −2.89 to −0.35, P= 0.013) and increase in TAC (SMD: 0.92, 95 % CI: 0.33–1.52, P = 0.002) following ω−3 fatty acids administration. Meanwhile, supplementation did not have beneficial effects on malondialdehyde, C-reactive protein (CRP), superoxide dismutase (SOD), and interlukin-6 levels. The subgroup analysis revealed a significant decrease in CRP levels and an increase in SOD levels in studies with durations of less than 12 weeks.

Conclusions

We found that ω−3 fatty acid intake can significantly decrease TNF-α and increase TAC levels, but this effect was not observed on other markers. Nevertheless, future well-designed with large sample size and long duration RCT studies with precise ω−3 fatty acids dose and ingredients are required to understand better the effects of these compounds and their constituents on oxidative stress and inflammatory markers in T2DM patients.

This systematic review and meta-analysis of randomized controlled trials (RCTs) sought to evaluate the effects of Nigella sativa (N. sativa) consumption on glycemic index in adults. A systematic literature search up to December 2023 was completed in PubMed, Scopus, and Web of Science, to identify eligible RCTs. Random effects models were assessed based on the heterogeneity tests, and pooled data were determined as weighted mean differences with a 95 % confidence interval. Finally, a total of 30 studies were found to be eligible for this meta-analysis. The pooled results using random effects model indicated that N. sativa supplementation significantly reduced FBS (SMD: −1.71; 95 % CI: −2.11, −1.31, p <0.001; I²= 92.7 %, p-heterogeneity <0.001) and HA1c levels (SMD: −2.16; 95 % CI: -3.04, −1.29, p <0.001; I²= 95.7 %, p-heterogeneity <0.001) but not effect on insulin (SMD = 0.48; 95 % CI: −0.53, 1.48, P = 0.353; I²= 96.1 %, p-heterogeneity <0.001), and HOMA-IR (SMD: −0.56; 95 % CI: −1.47, 0.35, p=0.229; I²= 95.0 %, p-heterogeneity <0.001).Overall, the evidence supports the consumption of N. sativa to reduce FBS and HA1c levels. Additional research, featuring extended durations and robust study designs, is necessary to determine the ideal dosage and duration of N. sativa supplementation for achieving a positive impact on glycemic markers.

Background

Altered biosynthesis of eicosanoids is linked to type 2 inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP), but their role in recalcitrant NPs is unclear.

Objectives

We sought to identify endotypes that are linked to recalcitrant CRSwNP, based on eicosanoids, their biosynthetic enzymes, and receptors as well as cytokines and the presence of eosinophils and mast cells in recurrent NPs.

Methods

Mucosal tissue collected at the time of sinus surgery from 54 patients with CRSwNP and 12 non-CRS controls were analysed for leukotriene (LT) E4, prostaglandin (PG) D2, 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) and 17 cytokines with ELISAs and Bio-Plex immunoassays. Patient subgroups were identified by cluster analysis and the probability of NP recurrence were tested with logistic regression analyses. Gene expressions were analysed with qPCR. Tryptase and eosinophil-derived neurotoxin (EDN) were measured with ELISAs as indications of the presence of mast cells and eosinophils, respectively.

Results

Clustering of patients showed that an inflammatory signature characterised by elevated LTE₄, PGD₂, 15(S)-HETE and IL-13 was associated with NP recurrence. Previous NP surgery as well as aspirin-exacerbated respiratory disease were significantly more common among these patients. Expression of cyclooxygenase 1 was the only gene associated with NP recurrence. Levels of EDN, but not tryptase, were significantly higher in patients with recurrent NPs.

Conclusion

Distinguishing endotypes that include LTE₄, PGD₂, 15HETE and conventional biomarkers of type 2 inflammation could help predict recurrent nasal polyposis and thus identify cases of recalcitrant CRSwNP.

Naringenin (NAR) has shown potential as a cancer treatment, reducing cell proliferation and invasion in soft tissue sarcomas like liposarcoma (LPS). This study investigates NAR's role and molecular mechanism. Bioinformatic analysis was performed to assess the expression level of genes in LPS based on the GEO dataset. The heat map and PPI of genes were also analyzed. MTT, wound healing, DAPI staining, and flow cytometry evaluated the cell viability, migration, and apoptosis. Besides, real-time PCR was used to measure the NAR's impact on the expression levels of EMT, apoptosis, inflammation, and metastasis-related genes. The results showed that NAR reduces cell viability, proliferation, and migration but induces apoptosis in LPS cells. RT-PCR results revealed that NAR is capable of regulating the expression level of the apoptosis, EMT, migration, and Inflammation-related genes. This study demonstrated that NAR may play a crucial role in reducing cell viability, inducing apoptosis, and attenuating migration in Sw872 LPS cells. Consequently, NAR might be a promising and efficient factor in the treatment of LPS.

Background and aim

Even though the role of D2 (ergocalciferol) on cardiovascular disease risk components has been studied, conflicting results have been reported. Moreover, no single study has studied all these parameters and the role of vitamin D2 individually has not been assessed; hence, this systematic review and meta-analysis of randomized controlled trials was conducted to assess the effect of vitamin D2 supplementation on lipid profile, anthropometric indices, blood pressure, and inflammatory and glycemic biomarkers in humans.

Methods

Web of Science, Scopus, PubMed/Medline, and Embase were searched from database inception to July 2024, and the random effects model, according to the DerSimonian and Laird method, was used to generate combined estimates of the intervention’s effect on the outcomes.

Results

After full-text analysis, 11 eligible articles were included in our meta-analyses. No statistically significant association was observed between vitamin D2 administration and BMI, WC, TC, HDL-C, LDL-C, TG, DBP or SBP; however, a statistically significant decrease in CRP (WMD: − 1.92 mg/dL, 95 % CI: − 3.30 to − 0.54, P = 0.006) and HbA1c levels (WMD: − 0.37 %, 95 % CI: − 0.66 to − 0.09, P = 0.009), and a non-statistically significant decrease in FBG (WMD: − 4.61 mg/dL, 95 % CI: − 14.71 to 5.47, P = 0.370, I2 = 90 %, P ˂ 0.001) and HOMA-IR (WMD: − 0.10, 95 % CI: − 0.17–0.03, P = 0.002) were detected.

Conclusion

In summary, our systematic review and meta-analysis discovered that vitamin D2 administration was associated with a statistically significant decrease in CRP and HbA1c levels, without a significant correlation with other outcomes.

Periodontitis is featured as the periodontium’s pathologic destruction caused by the host’s overwhelmed inflammation. Omentin-1 has been reported to be aberrantly downregulated in patients with periodontitis, but the specific regulation of Omentin-1 during the pathogenesis of periodontitis remains unclear. In this study, human periodontal ligament stem cells (hPDLSCs) were stimulated by lipopolysaccharide (LPS) from Porphyromonas gingivalis to establish an in vitro inflammatory periodontitis model. hPDLSCs were treated with recombinant human Omentin-1 (250, 500 and 750 ng/mL) for 3 h before LPS stimulation. Results revealed that Omentin-1 significantly inhibited LPS-induced inflammation in hPDLSCs through reducing the production of proinflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6) and downregulating the expression of Cox2 and iNOS. Meanwhile, Omentin-1 significantly enhanced alkaline phosphatase (ALP) activity and Alizarin red-stained area, accompanied by increasing expression osteogenic markers BMP2, OCN and Runx2, confirming that Omentin-1 restores osteogenic differentiation in LPS-induced hPDLSCs. In addition, the conditioned medium (CM) from LPS-induced hPDLSCs was harvested to culture macrophages, which resulted in macrophage polarization towards M1, while CM from Omentin-1-treated hPDLSCs reduced M1 macrophages polarization and elevated M2 polarization. Furthermore, Omentin-1 also inhibited LPS-triggered endoplasmic reticulum (ER) stress in hPDLSCs, and additional treatment of the ER stress activator tunicamycin (TM) partially reversed the functions of Omentin-1 on inflammation, osteogenic differentiation and macrophages polarization. In summary, Omentin-1 exerted a protective role against periodontitis through inhibiting inflammation and enhancing osteogenic differentiation of hPDLSCs, providing a novelty treatment option for periodontitis.

We reported that lysophosphatidic acid (LPA) is present at 0.8 μM in mixed human saliva (MS). In this study, we examined the distribution, origin, and enzymatic generation pathways of LPA in MS. LPA was distributed in the medium and cell pellet fraction; a true level of soluble LPA in MS was about 150 nM. The soluble LPA was assumed to be generated by ecto-type lysophospholipase D on exfoliated cells in MS from LPC that originated mainly from the major salivary gland saliva. Our results with the albumin-back extraction procedures suggest that a significant pool of LPA is kept in the outer layer of the plasma membranes of detached oral mucosal cells. Such pool of LPA may contribute to wound healing in upper digestive organs including oral cavity. We obtained evidence that the choline-producing activity in MS was mainly due to Ca²⁺-activated lysophospholipase D activity of glycerophosphodiesterase 7.