Table 1.

In vivo antioxidant activity of flavonoids.

Compounds	Experimental Approach	Key Results	Refs
Apigenin	CCl4-induced hepatotoxicity in mice	SOD, CAT, GSH-Px, and GSH levels increased.	[91]
		MDA level was decreased.
Apigenin	Kainic acid (KA)-induced excitotoxicity	GSH levels were increased.	[78]
Apigenin	STZ-induced diabetic cardiomyopathy	SOD and GPx activity were increased.	[81]
		Decreased GSH levels.
Apigenin	H2O2-induced rat hepatic stellate cells	SOD and GSH levels were enhanced.	[83]
		ROS, MDA, and NO levels were inhibited.
Apigenin	Diabetes-associated cognitive decline a diabetic rat model	Decreased the MDA content.	[82]
		Increased SOD activity and GSH level.
		Inhibited the activities of cNOS and iNOS.
Apigenin	Myocardial ischemia/reperfusion injury in mice	Significantly decreased MDA.
		Elevated SOD activity.
Catechin	Subacute chlorpyrifos-induced oxidative stress	Reduced MDA content.	[75]
		SOD, CAT, and GPx activities were increased.
Catechin	Type 2 diabetic erythrocytes	Decreased MDA.	[84]
		Increased GSH.
Hesperetin	Acetaminophen-induced hepatotoxicity	Increased levels of glutathione. Increased SOD and CAT activities.	[88]
		Reduced MDA levels.
Hesperetin	Streptozotocin-induced diabetic in rat	Increased GSH.	[86]
		Improved CAT, SOD, and GPx.
		Decreased levels of MDA.
		Reduced protein carbonyl.
Quercetin	Subacute-chlorpyrifos-induced oxidative stress	Decreased malondialdehyde levels.	[75]
		Enhanced SOD, CAT, and GPx.
Quercetin	Streptozotocin-nicotinamide-induced diabetic rats	Improved SOD, CAT, GPx.	[90]
		Increased mRNA expression levels.
		Ameliorated MDA levels.
Quercetin	Streptozotocin-nicotinamide-induced diabetic rats	Improved cardiac SOD-1, CAT, and GPx-1.	[85]
Quercetin	Myocardial ischemia reperfusion (IR) injuries	Reduced MDA content.	[80]
		Increased the activities of GSH, SOD, CAT, GSH-Px, GR.
Quercetin	Sodium-azide-induced hepatic and splenic oxidative stress in vivo	SOD and GPx activities were significantly increased.	[87]
		Considerably reduced MDA concentrations.
Rutin	Intestinal toxicity induced by methotrexate	Decreased TBARS and protein carbonyl.	[77]
		Increased SOD, catalase, and GSH.
Rutin	Alloxan-induced diabetic nephropathy	Increased SOD and catalase.	[76]
		Reduced lipid peroxidation.
		Downregulated endoplasmic reticulum stress markers GRP78 and CHOP.
Rutin	Gastric lesions induced by 50% ethanol	Significantly increased GSH-Px activity.	[79]
		Decreased the levels of thiobarbituric acid.
Resveratrol	Ethanol-induced oxidative stress in vivo	Increased SOD activity.	[92]
		Increased catalase.
		Increased glutathione peroxidase.
Resveratrol	Oxidative stress cardiomyopathy induced by doxorubicin	Reduced MDA content.	[93]
		Promoted SOD, CAT, and GPx activities.
		Increased GSH.
Resveratrol	Lipopolysaccharide-induced oxidative stress	Significantly reduced the level of TBARS.	[94]
		Significantly increased glutathione level and the superoxide dismutase.
Resveratrol	Hyperglycemia-induced renal tubular oxidative stress damage	Prevented the SOD activity downregulation and MDA upregulation.	[95]
		Significantly increased CAT levels.
		Modulates the SIRT1/FOXO3a pathway.
Resveratrol	Murine model of lipopolysaccharide (LPS)-induced pulmonary fibrosis	Decreased MDA levels.	[96]
		Increased total antioxidant activity, superoxide dismutase, and catalase activities.