Diabetes mellitus (DM) is a dysmetabolic disease characterized by chronic hyperglycemia. In the developed countries, DM is the commonest life style disease that affects both old and young age. Nod-like receptor protein-3 (NLRP3)-mediated pyroptosis may in fact aid in the development of diabetic complications. Quercetin is a natural flavonoid, can be present in natural foods and plants. Many studies have reported the antioxidant role of quercetin on different tissues, but its effects on NLRP3-mediated pyroptosis in diabetic lung are unclear. The current study aimed to assess quercetin’s protective effects on lung function, oxidative stress, and NLRP3-mediated pyroptosis in Wister rats exposed to streptozotocin (STZ)-induced DM. Forty male Wister rats were randomly allocated into four equal groups. The groups of rats were as follows: group 1 (G1) was kept under normal control conditions; G2 was injected I/P quercetin at a dose of 30 mg/kg b.wt., daily for 30 days; G3 and G4 were injected with a single dose of streptozotocin (STZ) 50 mg/kg b.wt. I/P to induce DM. After 72-h post diabetes induction, the rats of G4 were treated with quercetin as a manner in the second group. The results showed that quercetin ameliorates the pulmonary dysfunctions caused by DM through restoring the levels of glucose, insulin, and arterial blood gases, as well as the oxidative markers. Also, NLRP3-pyroptosis-mediated IL1β was inhibited. Quercetin also reduces the effect of DM on the lung by decreasing the pathological changes in the lung. In conclusion, NLRP3 inflammasome-induced pyroptosis may aggravate lung injury in diabetic rats. Quercetin has the potential to ameliorate diabetes induced pulmonary dysfunction by targeting NLRP3.

Wheat germ oil (WGO) is a well-known product with anti-inflammatory and antioxidant properties. The current study aimed to investigate the impacts of WGO against ethanol-induced liver and kidney dysfunction at the serum, anti-inflammatory, antioxidants and anti-apoptotic signaling pathways. Rats received saline orally as a negative control or WGO in a dose of 1.5 mL/kg (1400 mg/kg body weight orally) for 15 days. The affected group received ethanol 50% v/v 10 mL/kg (5 g/kg) body weight orally once a day for consecutive 15 days to induce hepatorenal injuries in ethanolic non-treated group. The protective group received WGO daily 1 h before ethanol administration. Serum (1.5 mL) from blood was extracted and examined for the changes in biochemical assessments in serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), bilirubin, serum γ-glutamyl transpeptidase (GGT), total protein, serum albumin, butyrylcholinesterase (BChE), total cholesterol (TC), total triglyceride (TG), urea, creatinine, uric acid, potassium (K+), Beta-2 microglobulin (β2M), malondialdehyde (MDA), catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD) and aspartate aminotransferase (AST). Kidney and liver homogenate was used to measure MDA, GSH and catalase activities. Quantitative real time PCR (qRT-PCR) was used to express Nrf2 and HO-1 in liver, and NF-kB and kidney injury molecule (KIM-1) in kidneys, which are correlated with oxidative stress and inflammation. Capase-3 and Bcl2 genes were examined using immunohistochemical analysis in the kidney and liver. Ethanol administration induced significant alteration in examined liver and kidney markers (AST, ALT, GGT, ALP, total proteins, urea, creatinine and uric acid). Moreover, alcohol administration decreased antioxidant activities at serum and hepatorenal tissues (GSH, catalase and SOD), while MDA was increased as a tissue degradation marker. Inflammatory cytokines, together with genes of oxidative stress markers (Nrf2 and HO-1), were all affected. At cellular levels, apoptotic marker caspase-3 was upregulated, while antiapoptotic marker B-cell lymphoma 2 (Bcl2), was down regulated using immunohistochemical analysis. Of interest, pretreatment with WGO improved the side effects induced by ethanol on hepatic, renal biomarkers and reversed its impact on serum and tissue antioxidant parameters. Nrf2/HO-1 were upregulated, while NFk-B and KIM-1 were downregulated using real time PCR. Immune reactivities of caspase-3 and Bcl2 genes were restored in the protective group. In conclusion, WGO ameliorated ethanol-induced hepatic and renal dysfunction at the biochemical, molecular and cellular levels by regulating some mechanisms that controls oxidative stress, apoptosis, inflammation and anti-apoptotic pathways.

Background: Diabetic nephropathy (DN) is a common complication among type II diabetic patients which may lead to end stage renal disease. Oxidative stress has been found to play a part in the pathophysiology of DN. Several studies have demonstrated the effective nephroprotective role of vitamin D to counteract the progression of DN, although the exact mechanisms are not yet fully understood. Adropin release has been recently linked to be one of the vitamin D effects and was reported to exert its antioxidant effects via nuclear factor erythroid 2-related factor 2 (Nrf2).Aim: To examine the nephroprotective effects of Vitamin D focusing on adropin-Nrf2 axis as one of the possible underlying mechanisms of vitamin D in rats. Materials and Methods:Thirty two albino male adult rats were used in this experiment. Rats were randomly and equally divided into four groups:(GI) was the control, (GII) received vitamin D, (GIII) was the diabetic model, and (GIV) was the diabetes+ vitamin D group. Results: Rats that received vitamin D (0.03 µg/kg/day) for 8 weeks revealed significant lower insulin resistance and oxidative stress state, a significant improvement of kidney dysfunction that was confirmed with histopathological examinations for kidney, and significantly higher levels of serum adropin in association with a significant higher renal mRNA expression of Nrf2. Conclusion: Vitamin D administration has a renoprotective effect in DN in type II diabetic rats. The antioxidant effects of vitamin D may be in part related to the adropin-Nrf2 axis.

Senile osteoporosis (SOP) is a degenerative bone disease associated with increasing susceptibility to fractures and mortality in the elderly. Innate immunity and specifically the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, with its subsequent mediators caspase1and interlukin-1b (IL-1b),have recently been linked to osteoporosis. Probiotic lactobacillus acidophilus (L.A) was reported to exert favorable effects on osteoporosis.The aim of this study was to identify the protective effects of probiotic L.A in aged osteoporotic rat model and to evaluate the possible underlying mechanisms focusing on NLRP3 inflammasome and its effectors caspase-1 and interleukin -1b. Thirty-two adult male albino rats were designated to four equivalent groups. Group I; control, group II; probiotic L.A, group III; osteoporotic group, and group IV; probiotic LA+ osteoporosis group. Osteoporotic rats pretreated with L.A in a dose of 10 9 CFU/ml / day for 8 weeks revealed a significantly lower oxidative stress state, increased bone mineral density (BMD), enhanced bone histological architecture, lower serum calcium, higher bone formation markers associated with lower bone resorption marker, lower serum receptor activator of nuclear factor kappa-Β ligand (RANKL), decreased bone NLRP3 inflammasome as well as caspase-1 expression levels and lower serum IL-1b.Osteoprotective effects of probiotic L.A in SOP rat model mediated even in part via its anti-inflammatory effects that was represented by decreased NLRP3 inflammasome and its subsequent mediators caspase-1 and IL-1b, that resulted in enhancement of bone formation and reduction of bone resorption.