Neuroprotection of Catalpol for Experimental Acute Focal Ischemic Stroke: Preclinical Evidence and Possible Mechanisms of Antioxidation, Anti-Inflammation, and Antiapoptosis

Table 4

Characteristics of mechanism studies of other compounds from Radix Rehmanniae on oxidation stress, anti-inflammation reactions, or apoptosis.

Study (years)	Model	Method of administration (experimental group versus control group)	Observations	Possible mechanisms
Liu [42]	Lipid peroxidation in rat liver microsome induced by Fe^2+-cysteine	Rehmaglutoside E versus no treatment	Decreased MDA content	Reduction of oxidative reactions
	Lipid peroxidation in rat liver microsome induced by Fe^2+-cysteine	6-O-E-Caffeoyl ajugol versus no treatment	Decreased MDA content	Reduction of oxidative reactions
	(1) Lipid peroxidation in rat liver microsome induced by Fe^2+-cysteine; (2) Inflammation in cells induced by LPS	Leucosceptoside A versus no treatment	(1) Decreased MDA content; (2) Decreased NO production	Reduction of oxidative reactions, repression of inflammatory reactions
	Lipid peroxidation in rat liver microsome induced by Fe^2+-cysteine	Jionoside D versus no treatment	Decreased MDA content	Reduction of oxidative reactions
	Inflammation in cells induced by LPS	Acteoside versus no treatment	Decreased NO production	Repression of inflammatory reactions
	Inflammation in cells induced by LPS	Salidrosid versus no treatment	Decreased NO production	Repression of inflammatory reactions
	Inflammation in cells induced by LPS	Jionoside D versus no treatment	Decreased NO production	Repression of inflammatory reactions
	Inflammation in cells induced by LPS	Jionoside B1 versus no treatment	Decreased NO production	Repression of inflammatory reactions
	Inflammation in cells induced by LPS	Vanillin versus no treatment	Decreased NO production	Repression of inflammatory reactions
Nan et al. [43]	Inflammation in mouse microglial cells induced by LPS	Ajugol versus no treatment	Decreased NO production	Repression of inflammatory reactions
Chai et al. [44]	Bile duct-ligated SD rats	Oleanolic acid versus saline	Decreased serum TNF-α, IL-1β, and IL-6	Repression of inflammatory reactions
			Decreased serum TBA, TBIL, DBIL, ALP, ALT, and AST; Reduced serum total bile acid and bile salt
Goyal et al. [45]	Cardiac toxicity rats induced by doxorubicin	Oleanolic acid versus no treatment	Decrease the activities of GSH, SOD, and catalase and MDA level	Reduction of oxidative reactions
			Decreased CK-MB, LDH, and heart weight; Improved alterations in ECG and histopathology of myocardium
Liu et al. [46]	Oxidative damage in PC12 cells induced by hydrogen peroxide	Geniposide versus no treatment	Increased the expression of Bcl-2 and HO-1, delayed the peak of cAMP level	Reduction of oxidative reactions
			Decreased apoptotic and necrotic cells and increased the viability of PC12 cells	Inhibition of apoptosis
Wang et al. [47]	(1) MCAO/2 h in SD rats; (2) Oxygen-glucose deprivation/4 h in primary microglial cell	Geniposide versus no treatment	(1) Reduced infarct volume and inhibited the activation of microglial cells in ischemic penumbra; (2) Decreased cell viability, the secretion of TNF-α, IL-1β,; IL-6, IL-8, and IL-10, the expression of TLR4, and NF-kBp65, TLR4 mRNA level, nuclear translocation of NF-kBp65	Repression of inflammatory reactions

ALP: alkaline phosphatase; ALT: alanine aminotransferase; AST: aspartate aminotransferase; bcl-2: B-cell lymphoma-2; cAMP: cyclic adenosine monophosphate; CK-MB: creatine kinase isoenzyme-MB; DBIL: direct bilirubin; ECG: electrocardiograph; GSH: glutathione; HO-1: heme oxygenase-1; IL: interleukin; LDH: lactate dehydrogenase; LPS: lipopolysaccharide; MCAO: middle carotid artery occlusion; MDA: malondialdehyde; NF-kBp65: nuclear transcription factors in rats Bp65; SD: Sprague Dawley; SOD: superoxide dismutase; TBA: total bile salts; TBIL: total bilirubin; TLR4: toll-like receptor 4; TNF-α: tumor necrosis factor-α.