Prostaglandins & other lipid mediators最新文献

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.

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Transient receptor potential melastatin 7 (TRPM7) has been emerged as a potent drug target for immunomodulation with ion conductance and kinase activities. The research is projected to characterize the influences of TRPM7 on the course of ulcerative colitis (UC) and dissect the latent response mechanisms. The in vivo murine model and in vitro cell model of UC were both stimulated by DSS. RT-qPCR and western blotting tested the abundance of TRPM7. Colonic damage was estimated by Hematoxylin-eosin staining, calculation of colon length, measurement of DAI and MPO assay kit. CCK-8 method and TUNEL staining severally ascertained cell activity and apoptosis. ELISA method assayed the inflammatory levels and relevant assay kits determined oxidative stress levels. FITC-dextran flux, immunohistochemistry, TEER as well as western blotting evaluated intestinal barrier function. Immunofluorescence staining and western blotting appraised NLR family pyrin domain containing 3 (NLRP3)-dependent pyroptosis. Depleted TRPM7 retarded inflammation, oxidative damage as well as intestinal barrier damage both in vitro and in vivo. TRPM7 reduction repressed the pyroptosis mediated by NLRP3 inflammasome. NLRP3 agonist nigericin partly abolished the protection elicited by TRPM7 silencing against inflammation, oxidative damage as well as intestinal barrier damage in vitro. Collectively, TRPM7 deletion might possess the therapeutic potential in UC, the working mechanism of which might involve the inactivation of NLRP3-dependent pyroptosis.

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.

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.

Periodontitis is a chronic infectious disease that affects the oral health of adults. Periodontal stem cells (PDLSCs) have good self-renewal and multipotential differentiation abilities to maintain the integrity of periodontal support structure and repair defects. This study aimed to elucidate the role of peroxisome proliferator activated receptor-γ co-activator 1-α (PGC-1α) in lipopolysaccharide (LPS)-induced PDLSCs and the underlying mechanisms related to predicated that pyrin domain (PYD)-only protein 1 (POP1). Notably downregulated PGC-1α and POP1 expression was observed in LPS-induced PDLSCs. PGC-1α or POP1 overexpression significantly reduced the inflammation and enhanced the osteogenic differentiation of LPS-treated PDLSCs. Particularly, PGC-1 bound to POP1 promoter region and upregulated POP1 expression. Moreover, POP1 knockdown ameliorated the impacts of PGC-1α overexpression on the inflammation and osteogenic differentiation in LPS-induced PDLSCs. Besides, PGC-1α inactivated NLRP3 signaling in LPS-treated PDLSCs, which was reversed by POP1 knockdown. Taken together, PGC-1α inhibits NLRP3 signaling through transcriptional activation of POP1, thereby alleviating inflammation and strengthening osteogenic differentiation of LPS-induced PDLSCs.

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.

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.