Prostaglandins & other lipid mediators最新文献

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.

Previous studies have shown prostaglandin E2 (PGE2) produced a marked increase in calcitonin secretion in human C-cells derived from medullary thyroid carcinoma. However, it’s unclear whether PGE2 can increase the growth of C cells. In this study, we use TT cells as a C cell model to investigate the effect of PGE2 on the growth of C cells. The results revealed that both PGE2 and arachidonic acid (AA) significantly increased the count of TT cells, whereas indomethacin and Dup697 reduced this count. Notably, an increase in the level of AA was associated with an increase in the number of proliferating TT cells, indicating a dose–response relationship. PGE2 and its receptor agonists (sulprostone and butaprost) enhanced the proliferation of TT cells. By contrast, 17-phenyl-trinor-PGE2 exerted no significant effect on TT cell proliferation, whereas L161982 suppressed it. The positive effect of AA on TT cell proliferation was inhibited by indomethacin, NS398, Dup697 (complete inhibition), and SC560. Both PGE2 and AA increased the level of p-STAT5a. The positive effect of AA on p-STAT5a was completely inhibited by Dup697 but not indomethacin, NS398, or SC560. Treatment with indomethacin or Dup697 alone reduced the level of STAT5a in TT cells. AA increased the level of STAT5a, but this effect was inhibited by indomethacin, NS398, and Dup697. Overall, this study confirms the effect of PGE2 on the proliferation of TT cells. This effect is likely mediated through EP2, EP3, and EP4 receptors and associated with an increase in p-STAT5a level within TT cells.

Clinical evidence suggests the beneficial effects of sumac on cardiovascular risk factors. However, these results are controversial. This systematic review and meta-analysis of randomized controlled trials (RCTs) was performed to determine the effect of sumac supplementation on cardiovascular risk factors in adults. The PubMed, Embase, Web of Science, and Cochrane databases were searched from inception to 30 December 2023 to identify RCTs that were published in English. Data were presented as weighted mean difference (WMD) and associated 95 % confidence interval (CI). The quality of the included trials was measured using the Cochrane Collaboration's modified risk of bias tool. A pooled analysis of 16 trials showed that sumac consumption led to a significant reduction in fasting blood glucose (WMD: −6.03 mg/dl; 95 % CI: −9.67 to −2.39), hemoglobin A1c (WMD: −0.45 %; 95 % CI: −0.59 to −0.31), triglycerides (WMD: −9.07 mg/dL; 95 % CI: −16.19 to −1.94), low-density lipoprotein cholesterol (WMD: −5.58 mg/dL; 95 % CI: −11.27 to −0.12), BMI (WMD: −0.22 kg/m²; 95 % CI: −0.38 to −0.05), weight (WMD: −0.85 kg; 95 % CI: −1.44 to −0.27), waist circumference (WMD: −0.54 cm; 95 % CI: −0.92 to −0.15), and diastolic blood pressure (WMD: −2.72 mmHg; 95 % CI: −4.16 to −1.29). High-density lipoprotein-cholesterol level also increased significantly (WMD: 3.69 mg/dL; 95 % CI: 1.81–5.57). The overall results support possible protective and therapeutic effects of sumac on cardiovascular risk factors in adults. Additional prospective studies are suggested using longer intervention periods and higher supplementation doses to confirm these results.

Background

1.5 million new HIV infections occurred in 2021, suggesting new prevention methods are needed. Inflammation increases the risk for HIV acquisition by attracting HIV target cells to the female genital tract (FGT). In a pilot study, acetylsalicylic acid (ASA/Aspirin) decreased the proportion of FGT HIV target cells by 35 %. However, the mechanism remains unknown.

Methods

Women from Nairobi, Kenya took low-dose ASA (81 mg) daily for 6-weeks. Free oxylipins in the plasma were quantified by high-performance liquid chromatography-tandem mass spectroscopy.

Results

Oxylipins from 9 fatty acid substrates were detected, with more than one analyte from 4 substrates reduced post-ASA. Summary analysis found ASA downregulated cyclooxygenase and lipoxygenase but not cytochrome P450 activity with a lower n-6/n-3 oxylipin profile, reflecting reduced inflammation post-ASA.

Conclusions

Inflammation is associated with increased lipoxygenase activity and HIV risk. Our data suggests ASA reduces inflammation through downregulation of oxylipins. Understanding how ASA reduces inflammation may lead to novel HIV prevention approaches.

There is controversial data on the impacts of bitter melon (Momordica charantia) supplementations on anthropometric indices. Thus, we aimed to clarify this role of bitter melon through a systematic review, and meta-analysis of the trials. All clinical trials conducted on the impact of bitter melon on anthropometric indices were published until August 2023 in PubMed, Web of Sciences, Scopus, Embase, and Cochrane Library web databases included. Overall, 10 studies with 448 individuals were included in the meta-analysis. Meta-analysis of 10 trials with 448 participants revealed no significant reductions in body weight (BW) (WMD: 0.04 Kg; 95 %CI: −0.16–0.25; P =0.651), body mass index (BMI) (WMD: −0.18 kg/m2; 95 %CI: −0.43–0.07; P =0.171), waist circumference (WC) (WMD: −0.95 cm; 95 % CI: −3.05–1.16; p =0.372), and percentage of body fat (PBF) (WMD: −0.99; 95 % CI: −2.33–0.35; p =0.141) following bitter melon supplementation. There was no significant impact of bitter melon supplementation on BW, BMI, WC, and PBF. More large-scale and high-quality RCTs are necessary to confirm these results.