Effect of omega-3 supplementation on lipid profile in children and adolescents: a systematic review and meta-analysis of randomized clinical trials.

PURPOSE: Dyslipidemia is considered as a known risk factor for cardiovascular disease. Yet various trials with wide ranges of doses and durations have reported contradictory results. We undertook this meta-analysis of randomized controlled trials (RCTs) to determine whether omega-3 supplementation can affect lipid profile in children and adolescents. METHODS: Cochrane Library, Embase, PubMed, and Scopus databases were searched up to March 2021. Meta-analysis was performed using random-effect method. Effect size was expressed as weighted mean difference (WMD) and 95% confidence interval (CI). Heterogeneity was assessed using the I2 index. In order to identification of potential sources of heterogeneity, predefined subgroup and meta-regression analysis was conducted. RESULTS: A total of 14 RCTs with 15 data sets were included. Based on the combination of effect sizes, there was a significant reduction in TG levels (WMD: -15.71 mg/dl, 95% CI: -25.76 to -5.65, P=0.002), with remarkable heterogeneity (I2=88.3%, P<0.001). However, subgroup analysis revealed that omega-3 supplementation significantly decreased TG only in studies conducted on participants ≤13 years old (WMD=-25.09, 95% CI: -43.29 to -6.90, P=0.007), (I2=84.6%, P<0.001) and those with hypertriglyceridemia (WMD=-28.26, 95% CI: -39.12 to -17.41, P<0.001), (I2=0.0%, P=0.934). Omega-3 supplementation had no significant effect on total cholesterol, HDL, and LDL levels. Also, results of nonlinear analysis showed significant effect of treatment duration on HDL status (Pnon-linearity=0.047). CONCLUSION: Omega-3 supplementation may significantly reduce TG levels in younger children and those with hypertriglyceridemia. Also, based on the HDL-related results, clinical trials with longer duration of intervention are recommended in this population.

The effects of acute sumatriptan treatment on renal ischemia/reperfusion injury in rat and the possible involvement of nitric oxide.

Renal ischemia/reperfusion (I/R) injury is a common pathological condition. Studies reported renal toxicity following administration of triptans, which are commonly used for treating migraine headaches. To investigate the effects of sumatriptan and the molecular mechanisms involved in renal I/R injury in rats, ischemia was induced by bilateral clamping of renal pedicles followed by 24 h of reperfusion. Sumatriptan was administered in three different doses (5, 10, and 20 mg/kg) before I/R injury induction. Biochemical and histopathological changes were evaluated. The contribution of nitric oxide in modulating the effects of sumatriptan was determined by administrating aminoguanidine at 50 mg/kg 60 min before I/R injury. The tissue level of nitrite, superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. Sumatriptan at 10 and 20 mg/kg increased the serum level of creatinine (Cr) and blood urea nitrogen (BUN) significantly. There was also a significant increase in nitrite level of animals that received 10 mg/kg sumatriptan. Co-administration of sumatriptan with aminoguanidine significantly decreased the BUN and Cr. Depletion of SOD level (P < 0.05) and elevation of serum levels of MDA (P < 0.001) indicated the involvement of oxidative stress in sumatriptan adverse effects. Overall, the administration of sumatriptan intensified renal I/R injury through activation of inducible nitric oxide synthase and oxidative responses in rats.

Targeting Mammalian Target of Rapamycin: Prospects for the Treatment of Inflammatory Bowel Diseases.

Inflammatory bowel disease (IBD) is a general term for a group of chronic and progressive disorders. Several cellular and biomolecular pathways are implicated in the pathogenesis of IBD, yet the etiology is unclear. Activation of the mammalian target of rapamycin (mTOR) pathway in the intestinal epithelial cells was also shown to induce inflammation. This review focuses on the inhibition of the mTOR signaling pathway and its potential application in treating IBD. We also provide an overview of plant-derived compounds that are beneficial for the IBD management through modulation of the mTOR pathway. Data were extracted from clinical, in vitro and in vivo studies published in English between 1995 and May 2019, which were collected from PubMed, Google Scholar, Scopus and Cochrane library databases. Results of various studies implied that inhibition of the mTOR signaling pathway downregulates the inflammatory processes and cytokines involved in IBD. In this context, a number of natural products might reverse the pathological features of the disease. Furthermore, mTOR provides a novel drug target for IBD. Comprehensive clinical studies are required to confirm the efficacy of mTOR inhibitors in treating IBD.

The protective effect of acute pantoprazole pretreatment on renal ischemia/reperfusion injury in rats.

Renal ischemia/reperfusion injury (IRI), which occurs in many pathological conditions, is associated with high rate of morbidity and mortality. Activation of inflammatory responses and oxidative stress contribute to induce organ damage following IRI. Pantoprazole, a proton pump inhibitor, which is mostly prescribed for gastroesophageal reflux disease (GERD) has been shown to exert anti-inflammation effects. In order to evaluate the effects of pantoprazole on renal ischemia/reperfusion injury, four different doses of pantoprazole (4.5, 9, 18, and 36 mg/kg) were administered 30 min before the induction of IRI in male Wistar rats. Serum concentration of creatinine and blood urea nitrogen (BUN) were measured to assess renal function. Histopathological changes, malondialdehyde (MDA) level and toll-like receptor 4 (TLR-4) expression in renal tissue were determined and compared to control group. The results revealed that pretreatment with 18 and 36 mg/kg of pantoprazole leads to the significant decline in serum creatinine and BUN levels and the severity of necrosis grade in comparison with control group (P < 0.05). Pantoprazole also reduced the MDA level and TLR-4 expression in renal tissue. In summary, pantoprazole attenuates renal injury following ischemia/reperfusion. This effect is mediated partially through inhibition of oxidative stress and TLR-4 signaling pathway.