Table 2.

Summary of in vivo studies of antioxidant activities of PCA.

Model	Method	PCA dose/route/duration	Major finding	Interpretation	Reference
Sprague-Dawley rat	STZ-induced T1DM (50 mg/kg, ip)	50, 100 mg/kg, po	(i) PCA decreased plasma MDA (ii) PCA decreased cardiac MDA (iii) PCA decreased mitochondrial ROS production	PCA deceased oxidative stress in T1DM rats	[30]
Sprague-Dawley rat	H2O2-induced oxidative damage in young and age rats	5 mg/kg/day for 7 days (ip)	(i) PCA improved scores during the passive avoidance testing (ii) PCA decreased MDA in brain of aged rat (iii) PCA increased GSH-PX activity	PCA promoted endogenous antioxidant enzymatic activities and inhibited ROS generation	[26]
Mice	D-galactose-induced ROS and AGEs	0.5%, 1%, or 2% in diet for 8 weeks	(i) PCA decreased ROS and protein carbonyl content (ii) PCA retained GSH content (iii) PCA decreased CML, pentosidine, sorbitol, fructose, and methylglycoxal level in brain	PCA had antiglycative and antioxidant activity by retaining GSH	[29]
Mice	Young and aged	5 and 10 mg/kg (ip) for 7 days	In aged rats   (i) PCA elevated splenic weight   (ii) PCA increased the activities of GSH-PX   (iii) PCA increased catalase (CAT) activity   (iv) PCA decreased malondialdehyde (MDA) level	PCA was a potential antiageing agent by promoting endogenous antioxidant enzymatic activities	[28]
Mice	STZ-induced DM (50 mg/kg/iv)	1%, 2%, and 4% in diet for 8 weeks	(i) PCA at all concentrations decreased cardiac and renal MDA level (ii) PCA at 2% and 4% increased cardiac and renal GSH level (iii) PCA at 2% and 4% decreased cardiac and renal GSSG formation (iv) PCA at 2% and 4% increased GPX and catalase activity in cardiac and renal tissues	PCA had an antioxidative effect through the restoration of endogenous antioxidants	[3]