Paper Title
Catechin-Elicited Adverse Effects in Chronic Kidney-Diseased Rats - Evidenced by a Biochemical Action Mechanism

Catechin (CTN) is abundantly present in fruits and beverages. (+)-Catechin is considered as a powerful free radical and reactive oxygen species scavenger among various flavonoid classes. Currently, chronic kidney disease (CKD) patients are amounting and the anti-hypertensive, anti-hyperlipidemic, antioxidative, and anticancer bioactivities of nutraceutics have been recently acknowledged. However, CTN also has been considered to act as a prooxidant. To understand if CTN is beneficial for CKD patients, the doxorubicin (DR)-CKD-rat model was used to investigate the in vivo prognosis of CKD rats when treated with CTN. Results indicated CTN caused collagen deposition, renal edema, and oxidative stress in the CKD rats, resulting in a high ratio of kidney to body weight (0.96 vs. 0.81 for the DRCKD control) (p < 0.001). CTN substantially raised the levels of blood urea nitrogen (BUN) (70.8  7.8 vs. 37.0  4.5 mg/dL) (p < 0.05), malondialdehyde (MDA) (58.2  3.0 vs. 25.3  2.5 M) (p < 0.001), and uric acid (UA) (4.4  0.3 vs. 3.4  0.3 mg/dL) (p < 0.05) without improving the expression of PPAR (0.76  0.04 vs. 0.74±0.03) (p < 0.05). Conclusively, CTN tends to aggravate CKD based on the findings being 1) ineffective to alleviate hypertriglyceridemia; 2) an active prooxidant; 3) able to stimulate MDA production; 4) able to accelerate protein catabolism and elevate serum BUN; 5) able to elevate UA; and 6) enhancing the collagen deposition, evidencing catechin to be unsuitable to treat CKD, at least the DRCKD. Keywords: Catechin; chronic kidney disease; hyperlipidemia;peroxisome proliferator-activated receptors  (PPAR)