Nonalcoholic fatty liver disease (NAFLD) is an inflammatory lipotoxic disorder with a prevalence of over 25% worldwide. However, safe and effective therapeutic agents for the management of NAFLD are still lacking. https://www.selleckchem.com/products/vo-ohpic.html We aimed to investigate the hepatoprotective effect and molecular mechanism of 4-acetylantroquinonol B (4-AAQB), a natural ubiquinone derivative obtained from the mycelia of Antrodia cinnamomea. RAW264.7 and J774A.1 cells were treated with 4-AAQB and then stimulated with LPS or tunicamycin (TM) for 24h. Inflammatory responses, markers of endoplasmic reticulum (ER) stress, and NOD-like receptor protein 3 (NLRP3) inflammasome were analyzed in both cell lines. In the applied in vivo model, male C57BL/6J mice were fed with chow or a methionine/choline-deficient (MCD) diet along with vehicle or 4-AAQB (10mg/kg, i.p. injected, once a day) for 10 consecutive days. Plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissues were analyzed using histological techniques; protein levels involved in ER stress, NLRP3 inflammasome, and inflammatory responses were measured. 4-AAQB significantly ameliorated the plasma levels of ALT and AST as well as the NAFLD activity score (NAS) in mice fed the MCD diet. In addition, 4-AAQB suppressed inflammatory responses, ER stress, and NLRP3 inflammasome activation, but increased the nuclear factor erythroid 2-related factor 2 (Nrf2) and Sirtuin 1 (SIRT1) signaling pathways in both in vitro and in vivo models. We suggest that 4-AAQB treatment might be a tangible therapeutic strategy in the management of NAFLD/NASH. We suggest that 4-AAQB treatment might be a tangible therapeutic strategy in the management of NAFLD/NASH.Doxorubicin (DOX) is an anthracycline antibiotic used in the fight against many types of cancer. Although it is quite effective for this purpose, its clinical use is limited by its severe side effects, highlighting the relevance of efforts to identify substances that act to minimize these effects. In this work, we sought to verify the ability of andiroba oil (AO) and a nanoemulsion of andiroba oil (AN) to lessen the side effects of DOX. The animals were separated into 7 groups with 6 animals each mice treated with AO (2000 mg/kg), AN (2000 mg/kg), the antineoplastic agent DOX (40 mg/kg), AO+DOX, AN+DOX and solvent controls was used of negative control (corn oil and nanoemulsion surfactant). AO and AN were administered for 14 consecutive days orally by gavage and on the 13th day, applied DOX by intraperitoneal route (i.p.), in order to evaluate the protective potential of andiroba. The animals were euthanized on the 15th day. Hematological, biochemical, histological, and immunohistochemical parameters were analyzed. Andiroba reduced several aspects of the severity of lesions caused by DOX, decreasing hematotoxicity and the severity of histological changes in the liver and kidneys, and reducing the frequency of apoptotic cell death. In many cases, AN showed greater efficacy than AO alone, reflecting the feasibility of using this nanotechnology to improve the pharmacokinetics of lipid compounds in the body. The study sheds new light on the therapeutic benefits of andiroba and suggests new ways for investigating how the quantity and quality of lipid compounds affect exposed organisms. Oxidative stress is considered the main event in the pathogenesis. of diabetic nephropathy (DN). Zamzam water, being natural alkaline with exceptional characteristics, is capable of enhancing antioxidant mechanisms. In this context; the present study has aimed to investigate the protective effects of zamzam water alone or in combination with gliclazide against the streptozotocin (STZ) induced DN model in rats. DN was initiated by a single intraperitoneal dose of STZ. Three days later, diabetic rats were classified into 5 groups; a normal control group, a diabetic control group, a group receiving gliclazide, a group receiving zamzam water, and a group receiving both gliclazide and zamzam water. Blood pressure (BP) and heart rate (HR) were determined. Then rats were euthanized and serum was isolated for assessment of glucose, insulin, kidney function tests and nitric oxide (NO). Furthermore kidney contents of malondialdehyde (MDA) and reduced glutathione (GSH) were estimated. Histopathology or renal tissues and immunohistochemistry of caspase 3 were determined. In addition, islets of Langerhans were separated from normal rats by collagenase digestion method to study the effects of zamzam water on insulin release in-vitro. Furthermore, chemical analysis of zamzam water has been done. Zamzam water significantly decreased STZ-induced hyperglycemia, BP, HR, oxidative stress biomarkers, impairment in renal functions (urea, creatinine, albumin), morphological changes in kidney and apoptosis. Likewise, zamzam water markedly elevated insulin levels both in in-vivo and in in-vitro experiments. The effects were more pronounced in combination with gliclazide. Zamzam water has a promising renoprotective effect against STZ induced DN through its anti-diabetic, antioxidant, anti-inflammatory and anti-apoptotic potentials. Zamzam water has a promising renoprotective effect against STZ induced DN through its anti-diabetic, antioxidant, anti-inflammatory and anti-apoptotic potentials.This study was aimed to explore the mechanism of rutaecarpine (RUT) on ethanol-induced gastric ulcer (GU) in mice by integrated approaches. At first, the efficacy was determined through the macroscopic and microscopic state of stomach tissue and the expression levels of GU-related factors. Then, the serum metabolomics method based on UPLC-Q-TOF/MS was used to explore the specific metabolites and metabolic pathways. Finally, the upstream key protein targets of these specific metabolites were analyzed by network pharmacology and verified by PCR to explore the potential mechanism. RUT alleviated the histological and pathological damage of gastric tissue caused by ethanol, and could remarkably ameliorate the level of GU-related factors. Subsequently, a total of 7 potential metabolites involved in 9 metabolic pathways were identified by metabolomics analysis. Then, a 'component-targets-metabolites' interaction network was constructed, and therefore 4 key target proteins (PLA2G1B, PDE5A, MIF and SRC) that may regulate the specific metabolites were obtained.