Lesion of the gastric mucosa is the most prevalent side effect of aspirin. Flavonoids with actions such as antioxidant, free radical scavenger and lipid peroxidant inhibitor can prevent mucosal lesion caused by aspirin. In this research effect of QUERCETIN, as the most abundant flavonoid in human diet, was investigated on preventing ulcerogenic effect of aspirin or Acetyl Salisylic Acid (ASA). Eighteen male Wistar rats (220-330gr) were randomly divided into 3 groups (6 in each group). In all groups consumption materials were adminstrated only once in acute form. First and second groups, as control groups, received ASA vehicle (1ml, orally) and ASA suspension (300mg/kg, 1ml, orally) respectively. The third group had a pretreatment with QUERCETIN (200mg/kg) half an hour before consumption of 300mg/kg ASA. After consumptiom the materials animals were kept 3hours, after that stomach was removed and was assessed for macroscopic and microscopis stomach mucosal lesions. Our results showed that, oral adminstration of ASA (300mg/kg) caused considerable stomach mucosal lesions (P<0.05) and pretreatment with QUERCETIN decreased the lesions (P<0.05). Therefore QUERCETIN can be effecttive in protecting stomach mucosa against ulcers caused by ASA. Although the mechanism of QUERCETIN action is not known, it might be used for mucosal protection with further investigations.

Introduction: Neonicotinoids are a new type of insecticides that have been introduced to the poison market during the last three decades. Acetamiprid (ACT) is a neonicotinoid and widely used for controlling pests. It targets the liver as a toxic agent and damages hepatic tissues through oxidative stress mechanisms. QUERCETIN is a flavonoid with potent antioxidant and hepatoprotective activity and protects tissues from oxidative damages. Thus, this study is aimed to assess the protective effect of QUERCETIN on acetamiprid-induced hepatotoxicity. Methods: Thirty-six Wistar rats were classified into six groups including control, DMSO, ACT 20, ACT 40, QUERCETIN, and ACT40+QUERCETIN. All treatments were administered orally with gavage for 28 days. Alanine amino transferase (ALT), aspartate amino transferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzyme activity was measured in serum as biomarkers of hepatotoxicity. Lipid peroxidation, superoxide dismutase (SOD) enzyme activity and total thiol content were measured in hepatic tissues. Also, hepatic tissue sections were prepared and stained with hematoxylin and eosin and evaluated under optic microscope for any tissue injuries. Results: Findings showed that ACT, especially in high dose (40mg/kg), induced hepatic tissue destruction associated with increased hepatic enzyme activity, except ALP activity, in the serum. Besides, ACT increased the lipid peroxidation and decreased total thiol content and SOD activity, which indicates ACT-induced oxidative stress in hepatic tissues. Also, hepatic tissue injuries were observed in ACT-treated group. All these changes in liver were prevented by QUERCETIN. Conclusion: Because of strong antioxidant properties, QUERCETIN can cope effectively with ACT-induced hepatotoxicity.

Purpose: QUERCETIN is a flavonoid known for its therapeutic properties and for forming complexes. Although the antimony-QUERCETIN (SbQ) complex has been produced before, no previous exploration of its characteristics has been published in literature. Thus, this study aimed to characterize this complex, assess its stability and investigate its complexation site through its antibacterial activity. Methods: The SbQ complex was synthetized using Sb(III) potassium tartrate trihydrate and QUERCETIN anhydrous (1: 1) (v/v) as a solution and dried using three methods: rotaevaporation, lyophilization and spray drying. The material, in solution, was analyzed by UV-vis and fluorimetry; and, in the powder, by X-ray diffraction (XRD), both scanning electronic and fluorescence microscopy and infrared spectroscopy (FT-IR). Antimicrobial activity was evaluated via broth microdilution. Results: UV-vis exhibited a shoulder peak at 291 nm indicating metal chelation at C-ring of QUERCETIN and confirmed 1: 1 stoichiometry. Spectrofluorimetry showed an increase of intensity with the complex formation with an emission band (525 nm). After drying, XRD and SEM indicated loss of crystallinity and a difference in shape and size of the complex compared to its precursors. FT-IR suggested by a shift of frequency of the carbonyl group (1661 cm-1) that the QUERCETIN bond to antimony by the C-3, followed by positions C-5 and C-4 carbonyl, which has been confirmed by MIC through the structure-activity relationship of the antibacterial activity of QUERCETIN. Conclusion: These results provided a characterization of SbQ complex with the confirmation of its binding site, working as a guide for future studies involving this complex.