NLRP3 inflammasome activation in macrophages fuels sterile inflammation, which has been tied with metabolic reprogramming characterized by high glycolysis and low oxidative phosphorylation. The key enzymes in glycolysis and glycolysis‐related products can regulate and activate NLRP3 inflammasome. In turn, NLRP3 inflammasome is considered to affect glycolysis, as well. However, the exact mechanism remains ambiguous. On the basis of these findings, the focus of this review is mainly on the developments in our understanding of interaction between NLRP3 inflammasome activation and glycolysis in macrophages, and small molecule compounds that influence the activation of NLRP3 inflammasomes by regulating glycolysis in macrophages. The application of this interaction in the treatment of diseases is also discussed. This paper may yield valuable clues for development of novel therapeutic agent for NLRP3 inflammasome‐related diseases.

Apples and their products exemplify the recently reemphasized link between dietary fruit intake and the alleviation of human disease. Their consumption does indeed improve human health due to their high phytochemical content. To identify potentially relevant articles from clinical trials, some epidemiological studies and meta‐analyses, and in vitro and in vivo studies (cell cultures and animal models), PubMed was searched from January 1, 2012, to May 15, 2022. This review summarized the potential effects of apple and apple products (juices, puree, pomace, dried apples, extracts rich in apple bioactives and single apple bioactives) on health. Apples and apple products have protective effects against cardiovascular diseases, cancer, as well as mild cognitive impairment and promote hair growth, healing of burn wounds, improve the oral environment, prevent niacin‐induced skin flushing, promote the relief of UV‐induced skin pigmentation, and improve the symptoms of atopic dermatitis as well as cedar hay fever among others. These effects are associated with various mechanisms, such as vascular endothelial protection, blood lipids lowering, anti‐inflammatory, antioxidant, antiapoptotic, anti‐invasion, and antimetastatic effects. Meanwhile, it has provided an important reference for the application and development of medicine, nutrition, and other fields.

Objectives. We aimed to investigate the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor on blood lipid levels in patients with high and very-high cardiovascular risk. Design. 14 trials (n = 52,586 patients) comparing treatment with or without PCSK9 inhibitors were retrieved from PubMed and Embase updated to 1st Jun 2021. The data quality of included studies was assessed by two independent researchers using the Cochrane systematic review method. All-cause mortality, cardiovascular mortality, and changes in serum low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglyceride (TG), apolipoprotein B (ApoB), lipoprotein (a) (LP (a)), non-high-density lipoprotein cholesterol (non-HDL-C), high-density lipoprotein cholesterol (HDL-C), and apolipoprotein A1 (ApoA1) from baseline were analyzed using Rev Man 5.1.0 software. Results. Compared with treatments without PCSK9 inhibitor, addition of PCSK9 inhibitors (evolocumab and alirocumab) had obvious decreasing effects on the levels of LDL-C [MD = −46.86, 95% CI (−54.99 to −38.72), ], TC [MD = −31.92, 95% CI (−39.47 to −24.38), ], TG [MD = −8.13, 95% CI (−10.48 to −5.79), ], LP(a) [MD = −26.69, 95% CI (-27.93 to −25.44), ], non-HDL-C [MD = −42.86, 95% CI (−45.81 to −39.92), ], and ApoB [MD = −38.44, 95% CI (−42.23 to -34.65), ] in high CVD risk patients. Conversely, changes of HDL-C [MD = 6.27, CI (5.17 to 7.36), ] and ApoA1 [MD = 4.33, 95% CI (3.53 to 5.13), ] from baseline were significantly more in high cardiovascular disease risk patients who received PCSK9 inhibitors treatment. Conclusion. Addition of PCSK9 inhibitors to standard therapy resulted in definite improvement in blood lipid levels compared with therapies that did not include them.

Rheumatoid arthritis (RA) is an autoimmune disease with an unclear pathogenesis. Granzyme B (GZMB) has been reported as a potential therapeutic target for RA treatment, but its mechanism remains unclear. This study aimed to explore the molecular mechanism of the GZMB-Caspase-3-GSDME pathway in the progression of RA. An SD rat model of RA was constructed, and Western blot analysis was used to verify the high expression of the GZMB gene in RA rats. Functional validation was then performed on two common RA cells, HFLS-RA cells and MH7A cells, by inhibiting the GZMB gene with the GZMB siRNA virus. Cell proliferation function was measured by CCK8 and EDU assays; cell pyroptosis markers were detected by the LDH assay; inflammation factor levels were measured by ELISA; and the expression of GZMB and pathway-related genes and proteins was measured by Western blot. After GZMB silencing, cell proliferation was decreased compared to the control group, and the inflammation factors IL-1b and IL-18, as well as the pyroptosis markers LDH, IL-1b, and IL-18, were all reduced. The GZMB-related proteins GZMB, caspase-3, and Gasdermin E (GSDME) were also decreased. Therefore, GZMB silencing reduces pyroptosis by inhibiting caspase-3 and Gasdermin E decomposition. In summary, GZMB silencing inhibits the activation of caspase-3 and Gasdermin E, thereby delaying inflammation in RA. The GZMB gene may be a potential therapeutic target for RA.