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Inflammation is the driving force of many inflammatory and autoimmune diseases, Pyroptosis is a process of cell death in response to excessive inflammation. Punicalin has been reported to have anti-inflammatory effects. However, the anti-pyroptosis is unknown. Hence, this study was aimed to research the inhibition of MG on LPS/ATP-induced pyroptosis in vitro.<br />Lipopolysaccharide (LPS)/ATP were used to simulate mouse J774A.1 cells to mimic the inflammatory response and the role of punicalin was examined. The secretion of proinflammatory cytokines was analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC), caspase-1, and GSDMD-N in LPS/ATP-stimulated cells were examined by Western blot. N-acetylcysteine (NAC) was used to validate the role of Punicalin.<br />Punicalin significantly blocked the production of endogenous ROS, reduced LPS/ATP-induced activation of NLRP3, caspase 1, ASC and GSDMD-N, IL-1b and IL-18 protein levels. Furthermore, N-acetylcysteine (NAC), an ROS scavenger, inhibited the LPS/ATP-stimulated activation of NLRP3 inflammasome mediated inflammation and pyroptosis.<br />Punicalin ameliorates LPS/ATP-induced pyroptosis in J774A.1 macrophages, the mechanism may involve downregulation of the ROS/NLRP3 inflammasome signaling pathway.<br />Punicalin ameliorates LPS/ATP-induced pyroptosis in J774A.1 macrophages, the mechanism may involve downregulation of the ROS/NLRP3 inflammasome signaling pathway.Several pro-inflammatory factors and proteins have been characterized that are involved in the pathogenesis of inflammatory diseases, including acute respiratory distress syndrome, chronic obstructive pulmonary disease, and asthma, induced by oxidative stress, cytokines, bacterial toxins, and viruses. Reactive oxygen species (ROS) act as secondary messengers and are products of normal cellular metabolism. Under physiological conditions, ROS protect cells against oxidative stress through the maintenance of cellular redox homeostasis, which is important for proliferation, viability, cell activation, and organ function. However, overproduction of ROS is most frequently due to excessive stimulation of either the mitochondrial electron transport chain and xanthine oxidase or reduced nicotinamide adenine dinucleotide phosphate (NADPH) by pro-inflammatory cytokines, such as interleukin-1β and tumor necrosis factor α. NADPH oxidase activation and ROS overproduction could further induce numerous inflammatory target prs against oxidative injury to combat pulmonary inflammation. Moreover, the cytotoxicity of oxidative stress and apoptotic cell death can be protected via the induction of HO-1 by these drugs. The main objective of this review is to focus on Chinese herbs and old drugs to develop anti-inflammatory drugs able to induce HO-1 expression for the management of pulmonary inflammatory diseases.<br />Candida species are infrequently grown in bile cultures. An association between biliary candidiasis and regional malignancy may exist. The role of fungus membranes in frequent biliary stent occlusion is also presented in this case series.<br />We retrospectively identified patients who underwent percutaneous trans-hepatic cholangiogram (PTC) for obstructive jaundice between January 2014 and January 2019. The results of bile cultures - obtained by PTC - for all patients were analyzed, and patients with fungus growth were determined; their medical records were reviewed.<br />A total of 71 patients with obstructive jaundice underwent PTC between January 2015 and January 2019. Five patients (all male; mean age 55.8 years) had candida species growth in bile cultures. Two patients were diagnosed with cholangiocarcinoma, one with adenocarcinoma of the head of the pancreas, one with gallbladder cancer, and one with locally advanced gastric adenocarcinoma. Formation of fungal balls predisposed to frequent PTC drain clogging. Eradication of Candida was achieved in 4 patients after 10 days to 3 weeks of antifungal therapy.<br />We present a case series of biliary candidiasis in patients with obstructive jaundice and regional malignancy. We suggest that patients with obstructive jaundice and regional malignancy should be screened for biliary candidiasis. Persistent cholestasis may be caused by the recurrent formation of fungal membranes (balls).<br />We present a case series of biliary candidiasis in patients with obstructive jaundice and regional malignancy. We suggest that patients with obstructive jaundice and regional malignancy should be screened for biliary candidiasis. Persistent cholestasis may be caused by the recurrent formation of fungal membranes (balls).The glutamic acid decarboxylase 65 antibody (GAD65-Ab) is an autoimmune marker in some diseases such as diabetes or autoimmune disorders of the central nervous system such as stiff-man syndrome. It can appear with other pancreatic autoantibodies, such as insulin autoantibodies (IAA), presenting as early signs of pancreatic islet β-cells impairing, and play roles in the pathogenesis of type1 diabetes (T1D) and latent autoimmune diabetes in adults (LADA). Positive GAD65-Ab is rarely observed in insulin-dependent diabetic patients with other acquired autoimmune diseases, such as Sjogren's syndrome (SS). Besides, LADA revealed by islet autoantibodies such as GAD65-Ab can also be complicated with Hashimoto's thyroiditis (HT), another autoimmune thyroid disease. To date, whether GAD65-Ab positive in patients with autoimmune diseases predicts the onset or progression to T1D or LADA remains unknown. Herein, two unique cases of middle-aged Chinese Han women free from diabetes for three years are described despite their blood tests persistently testing positive for GAD65-Ab or IAA. Both patients suffered from HT and SS. Follow-up OGTTs (oral glucose tolerance test) for three years revealed that the patients had a well-controlled glycemic level and normal pancreatic function. [https://www.selleckchem.com/products/rki-1447.html RKI-1447] However, one of the patients had a temporary increase of postprandial glucose after a short-term loss of diet control. The presence of auto-immune antibodies in these patients had little impact on glucose tolerance or insulin secretion in 3 years. The study postulate that both the primary immune injury caused by serum GAD65-Ab positive, an autoimmune marker, and increased body weight contribute to the progression of LADA.