Protective effect of quercetin on pulmonary dysfunction in streptozotocin-induced diabetic rats via inhibition of NLRP3 signaling pathway.

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 IL1ß 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.

Anti-inflammatory, anti-oxidant and hepatoprotective effects of lactoferrin in rats.

Carbon tetrachloride (CCl4) is a strong hepatotoxic agent. The ability of the anti-inflammatory agent, lactoferrin (LF), to alleviate hepatic inflammation in a Wistar rat model administered with carbon tetrachloride (CCl4) was examined. Thirty male Wistar rats were segregated into 5 groups (6 rats per group): Control group, LF group (300 mg LF/kg b. wt daily for three weeks), CCl4 group (1 ml CCl4/kg b. wt once orally), LF-protected group (300 mg LF/kg b. wt daily for 3 weeks followed by 1 mL CCl4/kg b. wt once orally), and LF-treated group (1 mL CCl4/kg b.wt once orally followed by 300 mg LF/kg b. wt orally every day for three weeks). Erythrogram, leukogram, activity of oxidative stress markers (Superoxide dismutase [SOD], Glutathione peroxidase [GPx], and Malondialdehyde [MDA]), and expression of hepatic paraoxonase-1 (PON1), interleukin (IL)-1ß, and IL-10 mRNA were determined. Histopathological examination of the hepatic tissue was carried out. CCl4 caused liver injury, loss of liver antioxidant activity of SOD and GPx, and a significant increase in the level of malondialdehyde in the serum. Moreover, CCl4 induced up-regulation of hepatic pro-inflammatory (IL-1ß) factors, and down-regulation of anti-inflammatory (IL-10 and PON1) factors. Based on histopathological examination, the hepatic tissues had severe inflammation and were damaged. However, LF mitigated the liver damage, oxidative stress, and hepatotoxicity caused by CCl4. Overall, these results suggest that LF-mediated immunological mechanisms alleviate CCl4-induced hepatic toxicity and provide a novel perspective on the potential use of LF for prophylactic and therapeutic applications in treating liver diseases.

Aflatoxicosis in cattle: clinical findings and biochemical alterations.

Aflatoxicosis is a serious health condition resulted from aflatoxin (AF)-producing fungi. Major health threats resulted from AFs and reflect on the livestock industry with great economic losses. There are limited scientific evidences concerning the AFs in ruminant, therefore it is important to evaluate AFs health hazards in cattle. Here, we investigate biochemical, oxidative stress, and postmortem changes associated with unexpected acute bovine aflatoxicosis. Seventy-two cattle were suffered from aflatoxisocis. Depression and inappetence were predominant clinical findings of the diseased animals. Analysis of feedstuffs revealed presence of aflatoxin B1 (AFB1). The AF-intoxicated animals showed a significant increase in alanine amino transferase (ALT), aspartate amino transferase (AST), alkaline phosphatase (ALP), serum creatinine (SCr), catalase (CAT), and malondialdehyde (MDA) levels. Moreover, a significant decrease in total protein (TP), magnesium (Mg), and reduced glutathione (GSH) were also seen. Hepatomegaly, enlarged gallbladder as well as congestion of the intestine and kidney were observed. This study elucidates the critical and constructive measurements needed for the prevention of the AFs hazardous effects to livestock for the future control of AF outbreaks. Conducting series of diagnostic assays reflect the marked health condition alterations in the biochemical and antioxidant status of the AF-intoxicated cattle.

Ameliorative effects of Moringa oleifera leaf extract on levofloxacin-induced hepatic toxicity in rats.

Fluoroquinolones are some of the most common antibiotics used by clinicians all over the world. Levofloxacin, a fluoroquinolone, is used therapeutically in numerous countries; however, it can cause an increase in liver function tests and liver dysfunction. The current study was designed to determine the effect of Levofloxacin (40 mg/kg body weight (b.wt.) daily for 2 weeks) on rat liver function and oxidative stress markers as well as to evaluate the potential hepatoprotective effects of Moringa oleifera leaf extract as a known antioxidant herb. M. oleifera leaf extract was found to improve the hepatic dysfunction induced by Levofloxacin by recovering liver enzymatic activities (alanine aminotransferase [ALT], aspartate aminotransferase [AST] and gamma-glutamyl transferase [GGT]) to normal levels. The extract also reversed the antioxidant imbalance as measured by catalase and superoxide dismutase activities as well as by reduced glutathione and malondialdehyde levels. Moreover, M. oleifera leaf extract induced anti-inflammation by improving the production of interleukin (IL)-10. Additionally, its presence attenuated the downregulation of IL-1 induced by Levofloxacin alone from hepatic tissue. It can be concluded that M. oleifera extract can help reduce the side effects caused by Levofloxacin administration.

Hepatoprotective and immunomodulatory effects of copper-nicotinate complex against fatty liver in rat model.

AIM: The current study was designed to evaluate the potential hepatoprotective and immunomodulatory effects of copper-nicotinate complex (CNC) against methionine- and choline-deficient diet (MCDD)-induced fatty liver in rats. MATERIALS AND METHODS: Forty male Wistar rats were randomly allocated into one of four equal-sized groups (G1-G4). The G1 group was fed a balanced diet and kept under normal conditions; the G2 group received CNC orally at a dose of 0.043 mg/kg body weight, 3 times/week for 4 weeks, and a balanced diet; the G3 group was fed an MCDD for 4 weeks; and the G4 group was fed an MCDD and administered CNC at the same dose and route as G2. Blood samples were collected for the determination of serum enzyme activity. After 4 weeks of treatment, liver specimens were collected for the evaluation of the oxidative/antioxidative markers, cytokine gene expression, and histopathological examination. RESULTS: CNC improved MCDD-induced liver dysfunctions by recovering serum alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase activities to their normal levels. The glutathione (GSH) level and superoxide dismutase (SOD) activity significantly decreased, while lipid peroxidation (as reflected by malondialdehyde [MDA]) markedly increased in the liver tissue of the MCDD group. After cotreatment with MCDD and CNC, the GSH level and SOD activity markedly increased and the MDA level significantly decreased to return to normal levels. After cotreatment with MCDD and CNC, significant downregulation of the mRNA expression of hepatic interleukin (IL)-1ß, IL-4, macrophage inflammatory protein-1α, and monocyte chemoattractant protein-1 genes was found. Moreover, CNC reduced fatty liver complications by reducing the number of hepatic vacuolations, degenerative changes in the hepatocytes, and hemorrhage. CONCLUSION: CNC has the potential to limit tissue injury and possibly prevent the progression to severe liver disease caused by an MCDD.