Study on improvement mechanism of caudatin on liver injury in rats
- VernacularTitle:告达庭对大鼠肝损伤的改善作用机制研究
- Author:
Zhihui CHANG
1
;
Yang BU
2
;
Qian LIU
2
;
Qian MA
2
;
Jie SONG
2
;
E SUN
2
;
Yingjie WEI
2
;
Yi LUO
3
;
Xiaobin TAN
4
Author Information
1. Third Clinical Medical College，Nanjing University of Chinese Medicine，Nanjing 210028，China;Dept. of Pharmacy，Lianyungang Hospital of TCM Affiliated to Nanjing University of Chinese Medicine，Jiangsu Lianyungang 222002，China
2. Third Clinical Medical College，Nanjing University of Chinese Medicine，Nanjing 210028，China;Jiangsu Branch of China Academy of Traditional Chinese Medicine/Key Laboratory of New Drug Delivery Systems of Chinese Materia Medica，Jiangsu Provincial Academy of Chinese Medicine，Nanjing 210028，China
3. Dept. of Oncology，the Affiliated Hospital of Integrated Chinese and Western Medicine，Nanjing University of Chinese Medicine，Nanjing 210028，China
4. Third Clinical Medical College，Nanjing University of Chinese Medicine，Nanjing 210028，China
- Publication Type:Journal Article
- Keywords:
endoplasmic reticulum stress;
caudatin;
inflammation;
liver injury;
diethylnitrosamine
- From:
China Pharmacy
2023;34(5):531-536
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the improvement mechanism of caudatin on liver injury of rats. METHODS SD rats were randomly divided into blank group， model group， caudatin low-dose and high-dose groups （25， 50 mg/kg）， with 6 rats in each group. Diethylnitrosamine （DEN） was injected intraperitoneally three times per week for eight weeks to establish liver injury model of rats. At 5th week of modeling， the rats received relevant medicine or 0.5% sodium carboxymethylcellulose intragastrically for 4 weeks. The levels of liver function indexes [alanine transaminase （ALT）， aspartate transaminase （AST）， total protein （TP） and total bilirubin （TBI）] and inflammatory factors [interleukin （IL-6）， tumor necrosis factor α （TNF-α）， IL-1β] in serum were detected； the histopathological morphological changes of rat liver were observed； the positive protein expressions of nuclear factor κB （NF-κB） and 78 kDa glucose regulatory protein （Grp78） in liver tissue were also determined； the expressions of endoplasmic reticulum stress-related protein Grp78， C/EBP homologous protein （CHOP）， activating transcription factor 6 （ATF6） and inositol requiring enzyme 1α （IRE1α） and the level of protein kinase R-like endoplasmic reticulum kinase robertluoyi@126.com （PERK） in liver tissue were detected. RESULTS Compared with blank group， serum levels of ALT， AST， TBI， IL-6， TNF-α and IL-1β and positive expressions of NF-κB and Grp78 in liver tissue as well as protein expressions of Grp78， CHOP， ATF6 and IRE1α， PERK protein phosphorylation level were all increased significantly in model group （P＜0.05）， while the serum level of TP was decreased significantly （P＜0.05）. The disordered structure of liver lobule， swollen liver cells， unclear intercellular boundary were observed and accompanied by inflammatory cell infiltration. Compared with model group， most of the above indexes were significantly reversed in caudatin groups （P＜0.05）； the structure of hepatic lobule was relatively complete and clear， the cells were arranged orderly， and the infiltration of inflammatory cells was also reduced. CONCLUSIONS Caudatin has a significant improvement effect against DEN-induced liver injury in rats， the mechanism of which may be associated with inhibiting endoplasmic reticulum stress and inflammatory reaction.
