RESUMO
BACKGROUND: Esophageal cancer is a malignant tumor with a low survival rate. Statins, commonly prescribed for their lipid-lowering effects, have been suggested to possess potential chemopreventive properties against various cancers, including esophageal cancer. OBJECTIVES: This systematic review studied the association between statin intake and esophageal cancer. METHODS: To conduct this systematic review and meta-analysis, we reviewed studies published between 1980 and June 2023 in Web of Science (WOS), Embase, MEDLINE/PubMed, Scopus, and Cochrane Library databases according to the PRISMA guidelines. Data extraction, quality assessment, and statistical analyses were performed using predefined protocols. We used various statistical tests conducted by Stata statistical software. Statistical significance was considered significant at p < 0.05. RESULTS: Twenty-one studies were collected and analyzed. The meta-analysis demonstrated that the odds ratio (OR) of esophageal cancer in patients treated with statins was 0.65 (95% CI: 0.57-0.75, p < 0.001) compared to the non-receiving group. The ORs for case-control and cohort studies were 0.67 (95% CI:0.54-0.83, p < 0.001) and 0.62 (95% CI:0.55-0.71, p < 0.001), respectively. The investigation into the relationship between the statins intake and the incidence of esophageal cancer did not reveal any indication of publication bias according to both Begg's test (p = 0.966) and Egger's test (p = 0.113). CONCLUSION: The results revealed that the odds of esophageal cancer in patients treated with statins decreased by 35% compared to patients not treated with statins. However, further well-designed prospective studies are needed to validate these findings and understand the underlying mechanisms of statins in preventing esophageal cancer.
RESUMO
BACKGROUND: Ischemia-reperfusion injury (IRI) is a well-known ailment that can disturb organ function. OBJECTIVES: This systematic review study investigated fisetin's effects and possible mechanisms in attenuating myocardial, cerebral, renal, and hepatic IRIs. METHODS: This systematic review included studies earlier than Sep 2023 by following the PRISMA statement 2020. After determining inclusion and exclusion criteria and related keywords, bibliographic databases, such as Cochrane Library, PubMed, Web of Science, Embase, and Scopus databases, were used to search the relevant studies. Studies were imported in End- Note X8, and the primary information was recorded in Excel. RESULTS: Fisetin reduced reactive oxygen species (ROS) generation and upregulated antioxidant enzymes, such as superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), and glutathione peroxidase (GPx), in ischemic tissues. Moreover, fisetin can attenuate oxidative stress by activating phosphoinositide-3-kinase-protein kinase B/Akt (PI3K/Akt) and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways. Fisetin has been indicated to prevent the activation of several pro-inflammatory signaling pathways, including NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) and MAPKs (Mitogen-activated protein kinases). It also inhibits the production of pro-inflammatory cytokines and enzymes like tumor necrosis factor-a (TNF-α), inducible-NO synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), interleukin-1ß (IL-1ß), IL-1, and IL-6. Fisetin attenuates IRI by improving mitochondrial function, anti-apoptotic effects, promoting autophagy, and preserving tissues from histological changes induced by IRIs. CONCLUSION: Fisetin, by antioxidant, anti-inflammatory, mitochondrial protection, promoting autophagy, and anti-apoptotic properties, can reduce cell injury due to myocardial, cerebral renal, and hepatic IRIs without any significant side effects.
RESUMO
Background: Rosacea is a multifactorial skin inflammatory disorder with an unknown cure. Genetics and environmental factors such as microorganisms are involved in the rosacea etiology, for example, Helicobacter pylori have been suggested in rosacea progression. The present study investigated the relationship between H. pylori eradication and rosacea patient's improvement. Materials and Methods: H. pylori infection was investigated in 60 rosacea patients and 65 sex- and age-matched healthy control through enzyme-linked immunosorbent assay (ELISA) and HpSag tests. After infection confirmation, randomly half of the rosacea patients were treated for H. pylori eradication (test), and others received standard treatment (control). HpSag and ELISA tests were repeated after infection eradication and disease flow was surveyed for 60 days. The groups were compared using the ANOVA (Analysis Of Variance) test at the significant level of P < 0.05. Results: At the baseline, the mean of immunoglobulin G (IgG) (59.27 ± 41.4 RU/mL) and immunoglobulin M (IgM) (11.55 ± 6.1 RU/mL) in rosacea patients was higher than the level of IgG (41.38 ± 54.33 RU/mL) and IgM (8.11 ± 8.91 RU/mL) in healthy control (P < 0.04) and (P < 0.01), respectively. Also, the values for H. pylori infection were positive in all patients and 10 healthy controls. The mean titer of IgM and IgG in the test and control patients groups were different at baseline and after treatment. Furthermore, in the test patients group, the mean of IgG was reduced in active rosacea after treatment, and 63.9% of active patients showed rosacea remission after H. pylori eradication. Conclusion: Data suggest the exacerbating role of H. pylori in rosacea, and its eradication along with other therapeutic methods causes rosacea improvement.
