Total saponins of Panax japonicus improve cancer cachexia in mice through inhibiting inflammatory response mediated by NF-κB
10.3969/j.issn.1001-1978.2018.04.019
- VernacularTitle:竹节参总皂苷通过抑制NF-κB介导的炎性反应改善小鼠肿瘤恶病质研究
- Author:
Zhi-Yong ZHOU
1
;
Ya-Xin CHEN
;
De-Hong LI
;
Ya-Nan SONG
;
Chang-Cheng ZHANG
;
Ding YUAN
Author Information
1. 三峡大学医学院
- Keywords:
total saponins of Panax japonicus;
cancer cachexia;
muscle metabolism;
fat degradation;
NF-κB pathway;
inflammatory reaction
- From:
Chinese Pharmacological Bulletin
2018;34(4):532-537
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the therapeutic effect of total saponins of Panax japonicus(SPJ)on cancer cach-exia in mice with colon adenocarcinoma. Methods BALB/c mice were subcutaneously inoculated with mu-rine colon adenocarcinoma CT26 cells to induce ca-chexia. The model animals were randomly divided into three groups: model group, SPJ low dose group and high dose group. Gavage started on the 4th day after inoculation, and the dosage regimen was as follows:the normal and model groups were given 10 mL·kg-1 saline, qd ×27; the low dose and high dose groups were treated with 20 and 60 mg·kg-1SPJ respective-ly, qd ×27. After treatment, the effects of SPJ on body weight, tibialis anterior muscle, gastrocnemius muscle,spleen and epididymal fat changes of cachexia mice were observed. HE and Western blot were used to measure the changes of cross section of gastrocnemius muscle fibers and the expression of NF-κB,PAX7 and MuRF1 protein level in the gastrocnemius and tibialis anterior muscle. Results Compared with model group, the administration of SPJ could effectively re-duce the weight loss (P <0.05), increase muscle mass (P<0.05) and decrease muscle tissue degrada-tion in cachexia mice. Meanwhile,SPJ significantly re-duced the levels of IL-1β and TNF-α in serum (P <0.05) and decreased the expression of NF-κB. Con-clusion SPJ can improve cancer cachexia in mice in a dose-dependent manner. The potential mechanism may be associated with the inhibition of NF-κB mediated in-flammatory factor expression.
