In vitro and In vivo Antioxidant Property of Novel 2-phenyl Quinazoline 4-(3H)-one Derivatives

Kusuma, Praveen Kumar

doi:10.13005/bbra/2141

Cited by 4 publications

(2 citation statements)

References 10 publications

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“…In our study, oral administration of Q-Br to the rats along with TAA intoxication for 15 weeks study has restored the oxidant/antioxidant balance of the liver through the inhibition of lipid peroxidation and enhancement of the production of endogenous antioxidant enzymes of hepatocytes. Reportedly, scientists showed the hepatoprotective activity of quinazoline derivatives via their enhancement activity of hepatocellular antioxidant enzymes ( Kusuma and Vedula, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective potential of a novel quinazoline derivative in thioacetamide-induced liver toxicity

Salama¹,

Kue

Mohamad

et al. 2022

Front. Pharmacol.

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Purpose: The compound quinazoline Q-Br, 3-(5-bromo-2-hydroxybenzylideneamino)-2-(5-bromo-2 hydroxyphenyl) 2,3-dihydroquinazoline-4(1H)-one (Q-Br) was evaluated for its antioxidant capacity and potential hepatoprotectivity against sub-chronic liver toxicity induced by thioacetamide in rats.Materials and Methods: Rats were assigned into five groups; healthy (normal) and cirrhosis control groups were given 5% Tween 20 orally, the reference control group was given a Silymarin dose of 50 mg/kg, and low-dose Q-Br and high-dose Q-Br groups were given a daily dose of 25 mg/kg and 50 mg/g Q-Br, respectively. Liver status was detected via fluorescence imaging with intravenous injection of indocyanine green (ICG) and a plasma ICG clearance test. Liver malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were also tested. The degree of fibrosis was determined histologically by hematoxylin and eosin and Masson’s Trichrome staining. The immunohistochemistry of liver tissue inhibitor of metalloproteinase (TIMP-1), matrix metalloproteinase (MMP-2), and alpha-smooth muscle actin (α-SMA) was performed.Results: Q-Br recorded mild antioxidant capacity, dose-dependent improvement in the liver status, and inhibition of oxidative stress compared to cirrhosis control. Histopathology notified a remarkable reduction in the degree of fibrosis. Immunohistochemistry revealed an obvious low expression of MMP-2 and α-SMA along with a higher expression of TIMP-1 in Q-Br- and Silymarin-treated livers.Conclusion: Q-Br treatment altered the course of toxicity induced by thioacetamide suggesting significant hepatoprotective potential of Q-Br treatment.

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Section: Discussionmentioning

confidence: 99%

Hepatoprotective potential of a novel quinazoline derivative in thioacetamide-induced liver toxicity

Salama¹,

Kue

Mohamad

et al. 2022

Front. Pharmacol.

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“…Glutathione peroxidase (GPx) was determined following the methods of Kusuma and Vedula, [2016]. 50µl of 10% spleen homogenate in PBS (pH = 7.4) was taken in a test tube and mixed with 450µl of water.…”

Section: Evaluation Of Glutathione Peroxidase (Gpx) Activity Level In Spleenmentioning

confidence: 99%

Effect of Melatonin and Insulin on Oxidative Stress in Spleen, Impairment of Adherent Leukocytes Activity and Inflammatory Response in Lps Treated Diabetic Mice

Sutradhar

Deb

Singh

2021

Preprint

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The present study evaluated the protective effect of melatonin and insulin from LPS and diabetes-induced oxidative stress, impairment of peritoneal leukocyte functions, and inflammation in Swiss albino mice. Diabetes was induced in Swiss albino mice by streptozotocin treatment. Experimental mice were divided into two sets. Set-1 contains control, diabetic, melatonin, insulin, and melatonin+insulin groups of mice. In set-II, all groups of mice were challenged with a single dose of LPS (50mg/mice). Lipid peroxidation, antioxidant enzymes (SOD, Catalase, GPx) activity, non-enzymatic GSH level, Nrf2/HO-1 expression, phagocytic index, intracellular ROS generation, and proinflammatory cytokines were measured. Diabetic as well as LPS treated diabetic mice showed significantly increased lipid peroxidation, suppressed antioxidant defence system, and down regulated Nrf2/HO-1 expression in spleen tissues; suppressed phagocytic index and increased ROS generation in adherent peritoneal leukocytes and increased level of circulatory proinflammatory cytokines. Either treatment of melatonin or insulin significantly improved the harmful effects caused by both of LPS treatment and of diabetes in experimental mice. Simultaneous treatment of melatonin and insulin effectively ameliorated the LPS, as well as diabetes, caused oxidative load, impairment of adherent peritoneal leukocyte function, and improved the level of circulatory proinflammatory cytokines. In the present study, we have noted that combined treatment of melatonin and insulin was more effective in attenuation of diabetes and LPS induced devastating effects in laboratory mice. Therefore, the present study may suggest a combinatorial approach in the therapeutic use of melatonin and insulin to improve such devastating conditions.

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Protective efficacy of melatonin and insulin against LPS caused toxicity in diabetic mice

Sutradhar

Deb

Singh

2022

Immunopharmacology and Immunotoxicology

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In vitro and In vivo Antioxidant Property of Novel 2-phenyl Quinazoline 4-(3H)-one Derivatives

Cited by 4 publications

References 10 publications

Hepatoprotective potential of a novel quinazoline derivative in thioacetamide-induced liver toxicity

Hepatoprotective potential of a novel quinazoline derivative in thioacetamide-induced liver toxicity

Effect of Melatonin and Insulin on Oxidative Stress in Spleen, Impairment of Adherent Leukocytes Activity and Inflammatory Response in Lps Treated Diabetic Mice

Protective efficacy of melatonin and insulin against LPS caused toxicity in diabetic mice

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