Metformin Can Be Safely Used in Patients Exposed to Contrast Media: A Systematic Review and Meta-Analysis.

BACKGROUND: There have been few studies published on the use of contrast media (CM) in metformin-treated patients. In this study, we conducted a systematic review and meta-analysis to investigate the relationship between metformin and contrast-induced acute kidney injury (CI-AKI). METHODS: A comprehensive search of the Medline, PubMed, Embase, and Web of Science databases for literature on associations between metformin use and CI-AKI incidence was conducted. The pooled odds ratio (OR), or relative risk, as well as the corresponding 95% confidence intervals (CIs), was calculated to assess the relationship between metformin and CI-AKI risk as well as the incidence of lactic acidosis (LA). RESULTS: In total, seven studies met our eligibility criteria on associations between metformin use and CI-AKI incidence, comprising 2,325 individuals, with 279 new cases of CI-AKI exposed to CM. The pooled analysis revealed no statistically significant increase in the risk of CI-AKI development in patients who used metformin continuously (random-effects OR: 1.15, 95% CI: 0.70-1.90, p = 0.57). No cases of LA that occurred during CM exposure were reported. CONCLUSION: Metformin can be safely used in patients with moderate renal impairment (eGFR ≥ 30 mL/min/1.73 m2) during CM exposure.

Effects of Surgical Masks on Patients with Stable Chronic Heart Failure.

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TPPU, a sEH Inhibitor, Attenuates Corticosterone-Induced PC12 Cell Injury by Modulation of BDNF-TrkB Pathway.

High level of corticosterone (CORT) is toxic to neurons and plays an important role in depression-like behavior and chronic stress. Our previous study showed that TPPU, a soluble epoxide hydrolase (sEH) inhibitor (sEHI), induces an antidepressant effect in animal models. However, the underlying mechanism is not clear. In this study, we investigated the protective effect of TPPU on PC12 cells against CORT-induced cytotoxicity and its underlying mechanism. We found that TPPU and the sEH substrate epoxyeicosatrienoic acids (EETs) protected PC12 cells from the CORT-induced injury by increasing cell viability and inhibiting apoptosis. Furthermore, TPPU and EETs also blocked the CORT-mediated downregulation of BDNF. Blocking the BDNF-TrkB pathway by the TrkB inhibitor K252a abolished the protective effect of TPPU. Taken together, our results suggest that sEHI could protect PC12 cells against the CORT-induced cytotoxicity via the BDNF-TrkB signaling pathway.