Recent studies have shown that the composite of semiconductor photocatalytic materials and g-C3N4 can effectively inhibit photocatalytic carrier recombination and enhance the adsorption performance of the composite photocatalytic materials, so that the composite photocatalyst has stronger photocatalytic activity. In this paper, three kinds of graphitic carbon nitride photocatalyst g-C3N4 with different morphologies were prepared using the same precursor system by the chemical cracking method. After characterization and application, the sample with the most significant photocatalytic activity was selected and the g-C3N4/BiVO4 heterostructure was synthesized by the simple solvent evaporation method, then the photocatalytic experiment was carried out. The results show that, when the content of BiVO4 in the composite sample is 1%, the photocatalytic activity of RhB was the highest, and the degradation rate could reach 90.4%. The kinetic results showed that the degradation of RhB was consistent with the quasi-primary degradation kinetic model. The results of the photocatalytic cycle experiment show that the photocatalytic performance remains unchanged and stable after four photocatalytic cycles. The existence of a g-C3N4/BiVO4 binary heterojunction was confirmed by UV/Visible diffuse reflection (UV-DRS) and photoluminescence (PL) experiments. Owing to the Z-type charge process between BiVO4 and g-C3N4, efficient carrier separation was achieved, thus enhancing the photocatalytic capacity. This work provides a new idea for the study of heterojunction photocatalytic materials based on g-C3N4.
Cerebral ischaemia reperfusion (CIR) affects microRNA (miR) expression and causes substantial inflammation. Here, we investigated the influence and underlying mechanism of miR‐27a‐3p in rats with CIR. First, biliverdin treatment relieved cerebral infarction and decreased the levels of serum interleukin (IL)‐1β, IL‐6, and TNF‐α. Through our previous study, we found key miR‐27a‐3p and its targeted gene LITAF might involve in the molecular mechanism of CIR. Then, the regulation between miR‐27a‐3p and LITAF was verified by the temporal miR‐27a‐3p and LITAF expression profiles and luciferase assay. Moreover, intracerebroventricular injection of the miR‐27a‐3p mimic significantly decreased the LITAF, TLR4, NF‐κB, and IL‐6 levels at 24 h post‐surgery, whereas miR‐27a‐3p inhibitor reversed these effects. Furthermore, miR‐27a‐3p mimic could relieve cerebral infarct and neurologic deficit after CIR. In addition, injection of miR‐27a‐3p mimic decreased neuronal damage induced by CIR. Taken together, our results suggest that miR‐27a‐3p protects against CIR by relieving inflammation, neuronal damage, and neurologic deficit via regulating LITAF and the TLR4/NF‐κB pathway.
Due to the excellent antioxidant capacity of proanthocyanidins, combined with the antioxidant mechanism of anthocyanins, it inspired us to study the antioxidant capacity of proanthocyanidins and their complexes. In this article, we conducted antioxidant tests on proanthocyanidin-bovine serum albumin and procyanidin-metal complexes, using DPPH and ABTS methods to determine the antioxidant capacity of procyanidins and their complexes. The results show that compared with proanthocyanidins, the proanthocyanidin complex has a certain degree of improvement in the ability to scavenge free radicals. After being combined with metal ions, the ability to scavenge free radicals is significantly improved. When the ratio of proanthocyanidin B2 to Fe3+ is 2:1, the ability to scavenge free radicals is significantly enhanced.
Background Myocardial reperfusion injury is often accompanied by cell death and inflammatory reactions. Recently, pyroptosis is gradually recognized as pivotal role in cardiovascular disease. However, little is known about the regulatory role of beclin1 in the control of caspase-4 activation and pyroptosis. The present study confirmed whether beclin1 regulates caspase-4 mediated pyroptosis and thereby protects Cardiac microvascular endothelial cells (CMECs) against injury.Methods TTC and Evan's blue dye, western blot, immunofluorescence and immunohistochemistry staining were performed in wild mice and transgenic mice with overexpression of beclin-1(BECN1-Tg). CMECs were transfected with a beclin1 lentivirus. The cell cytotoxicity was analyzed by LDH-Cytotoxicity Assay Kit. The protein levels of autophagy protein (Beclin1, P62 and LC3II/LC3I) and caspase-4/GSDMD pathway were determined by western blot. Autophagic vacuoles in cells were monitored with RFP-GFP-LC3 using fluorescence microscope.Results I/R caused caspase-4 activity and gasdermin D expression increase in vivo and in vitro. Overexpression of beclin-1 in heart tissue and CMECs suppressed the caspase-4 activity and decreased the levels of gasdermin D; meanwhile beclin1 overexpression also reduced IL-1β levels, promoted autophagy (P62 expression was inhibited while LC3II expression was increased) in the heart and CMECs. Interestingly, beclin1 overexpression increased animal survival and attenuated myocardial infarct size post-myocardial ischemia reperfusion.Conclusions Induction of beclin-1 signaling can be a potential therapeutic target in myocardial reperfusion-induced microvascular injury.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.