Yi Qi Qing Re Gao formula ameliorates puromycin aminonucleoside-induced nephrosis by suppressing inflammation and apoptosis.
Wen Y1,2,3, Zhan Y4, Liu H5, Zhao T6,7, Yang L8, Zhang H9,10, Dong X11,12, Li P13,14.
Author information
1Beijing University of Chinese Medicine, Beijing, 10029, China. colline0725@163.com.2Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, 10029, China. colline0725@163.com.3Beijing Key Lab for Immune-Mediated Inflammatory Diseases, Beijing, 10029, China. colline0725@163.com.4Department of Nephrology, Guang’anmen Hospital of China Academy of Traditional Chinese Medical Sciences, Beijing, 100053, China. zhanyongli88@sina.com.5Department of Nephrology, Shunyi Hospital of Traditional Chinese Medicine, Beijing, 101300, China. liuhuijie66@163.com.6Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, 10029, China. ttfrfr@163.com.7Beijing Key Lab for Immune-Mediated Inflammatory Diseases, Beijing, 10029, China. ttfrfr@163.com.8Department of Nephrology, Guang’anmen Hospital of China Academy of Traditional Chinese Medical Sciences, Beijing, 100053, China. relyssia@gmail.com.9Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, 10029, China. zhhj529@163.com.10Beijing Key Lab for Immune-Mediated Inflammatory Diseases, Beijing, 10029, China. zhhj529@163.com.11Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, 10029, China. yaolishi2001@163.com.12Beijing Key Lab for Immune-Mediated Inflammatory Diseases, Beijing, 10029, China. yaolishi2001@163.com.13Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, 10029, China. lp8675@163.com.14Beijing Key Lab for Immune-Mediated Inflammatory Diseases, Beijing, 10029, China. lp8675@163.com.
Abstract
BACKGROUND:
Yi Qi Qing Re Gao (YQQRG) formula is a traditional Chinese herbal medicine used to treat chronic nephritis. This study was designed to evaluate the underlying mechanism in the use of YQQRG formula to treat nephrosis induced by puromycin aminonucleoside (PAN).
METHODS:
Thirty-six male Wistar rats were randomly divided into 3 groups of 12 rats each: a sham group, a vehicle-treated PAN model group (PAN), and a group treated with YQQRG (PAN + YQQRG). The PAN model was established by a single intravenous injection of PAN at a dose of 40 mg/kg body weight; rats in the sham group received the same volume of saline. Twenty-four hour urinary protein was measured 0, 3, 5, 10, and 15 days after the injection. The rats were sacrificed on day 10 and day 15 and the serum lipid profile examined. The renal cortex of each rat was stained with periodic acid-Schiff reagent and the pathologic alterations and ultrastructural changes were examined by transmission electron microscopy. In situ cell apoptosis was detected by a terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end-labeling (TUNEL) assay. Transcriptive levels of inflammatory markers and molecules associated with apoptosis were detected by a real-time polymerase chain reaction and expression of proteins was examined by either immunohistochemistry or Western blot analysis.
RESULTS:
YQQRG significantly decreased urinary protein level, and lowered serum lipid level. YQQRG also attenuated histologic lesions in the rat kidneys. Activation of inflammatory markers was largely restored by the administration of YQQRG. TUNEL assay showed that YQQRG decreased the number of apoptotic cells. Both mRNA and protein levels of caspase-3 were significantly reduced in the group treated with YQQRG, whereas expression of the Bcl-2 protein increased in the YQQRG group.
CONCLUSIONS:
YQQRG alleviated kidney injury in PAN-treated rats, possibly through anti-inflammatory and anti-apoptotic effects.