Anti-Macrophage monoclonal antibody [PE]

In this study, a polysaccharide (CGP-BG) was successfully produced from waste distillers' grain by Chaetomium globosum CGMCC 6882. Chemical analysis demonstrated that CGP-BG contained 3.49 +/- 0.51 % protein. The molecular weight of CGP-BG was 52.37 KDa, which was composed of rhamnose, arabinose, galactose, glucose, xylose, mannose, galactumnic acid, and glucuronic acid in the molar ratio of 4.11:7.34:13.31:20.99:1.07:0.91:4.75:0.36. In vitro assay showed that CGP-BG had scavenging activities on hydroxyl radical, DPPH radical, superoxide anion, and ABTS radical in a dose-dependent manner. Meanwhile, CGP-BG significantly inhibited nitric oxide and pro-inflammatory cytokine (TNF-alpha, IL-6, and IL-1 beta) production in the lipopolysaccharide (LPS)-induced RAW 264.7 cells. Moreover, CGP-BG notably improved the antioxidant status of LPS-treated macrophages by enhancing superoxide dismutase, glutathione peroxidase, and antioxidant capacity and mitigating malondialdehyde. This work provided the basis for the application of CGP-BG as an anti-inflammatory and antioxidant agent.

Pyroptosis is a pro-inflammatory type of regulated cell death (RCD) characterized by gasdermin D (GSDMD)mediated membrane pore formation, cell swelling and rapid lysis, followed by the massive release of pro-inflammatory mediators such as interleukin-1 beta and interleukin-18. There are two main pathways of pyroptosis: the caspase-1-mediated canonical pathway and the caspase-4/5/11-mediated noncanonical pathway. However, the caspase-3-gasdermin E (GSDME) pathway and caspase-8-GSDMD pathway also induce pyroptosis. Pyroptosis can not only cause local inflammation but also lead to amplification of the inflammatory response. Recent studies have suggested that pyroptosis is closely related with cardiovascular disease (CVD); for example, in atherosclerosis, myocardial infarction, ischemia-reperfusion injury, heart failure, coronary calcification and aortic aneurysm, study results have promoted the development of inhibitors targeting the components related to pyroptosis, and some agents have been clinically proven to have cardiovascular benefits. In this review, we summarize emerging evidence to discuss the progressive understanding of pyroptosis and the pathways, effect and effectors of pyroptosis, as well as the role of pyroptosis in CVD. Additionally, we summarize pyroptosis-related pathway inhibitors and classic cardiovascular drugs targeting pyroptosis.