Abstract:Objective To observe the anti-tumor and anti-inflammatory effect of asperuloside on mice with Lewis lung cancer, and to investigate the anti-inflammatory mechanism by which asperuloside inhibits the overactive tlr4/myd88/nf-κb pathway. Methods Thirty-six healthy c57bl/6j mice of SPF grade, after one week of adaptive feeding, underwent subcutaneous injection of Lewis cells under the armpits to establish a tumor-bearing model before they were randomly divided into the model control group, asperuloside group and cisplatin control group. Corresponding intervention was implemented, such as orally taking asperuloside or intraperitoneal injection of cisplatin, once a day for 3 weeks. After the last dose, the health status of these mice was observed, body mass and tumor mass measured, and their peripheral blood was collected. Levels of il-1β and tnf-α in serum were detected by ELISA. The expression levels of tlr4, myd88 and nf-κb in tumor tissues were measured with Western-blot technology. The localization and level of p-nf-κb in tumor tissues were measured by immunohistochemical technology. Results There was no significant difference in body weight between the three groups before administration. After administration, the weight of mice in the asperuloside group increased (P<0.01) compared with the model control group, and the difference was statistically significant. Compared with the asperuloside group, the weight of mice in the cisplatin control group was reduced (P<0.01) and the difference was also statistically significant. Compared with the model control group, the tumor index of mice in the asperuloside group and cisplatin control group was reduced (P< 0.01), and the difference was statistically significant. Compared with the model control group, the serum contents of il-1β and tnf-α were decreased(P<0.01), so were the expression levels of tlr4, myd 88, nf-κb and p- nf-κb in tumor tissues (P<0.01), and the difference was statistically significant. Conclusions Asperuloside can reduce inflammatory response in Lewis tumor- bearing mice.
Yinghan Chan,Sin Wi,Joycelin Zhu, et al. Emerging therapeutic potential of the iridoid molecule, asperuloside: a snapshot of its underlying molecular mechanisms[J]. Chem Biol Interact,2020,315(5):1-10.
[3]
Liao Y,Xu L,Lin X,et al.Temporal trend in lung cancer burden attributed to ambient fine particulate matter in Guangzhou,China[J].Biomed Environ Sci,2017,30(10):708-717.
[4]
Sigismund S,Avanzato D,Lanzetti L.Emerging functions of the EGFR in cancer[J].Mol Oncol,2018,12(1):3-20.
[5]
Gazdar A F,Bunn P A,Minna J D.Small-cell lung cancer:what we know,what we need to know and the path forward[J].Nat Rev Cancer,2017,17(12): 725-737.
He Jingyu,Lu Xianyuan,Wei Ting, et al. Asperuloside and asperulosidic acid exert an anti-inflammatory effect via suppression of the NF-κB and MAPK signaling pathways in LPS-Induced RAW 264.7 macrophages[J]. Int J Mol Sci, 2018,19(2027):1-12.
[9]
Qiu Jiaming,Chi Gefu,Wu Qianchao, et al.Pretreatment with the compound asperuloside decreases acute lung injury via inhibiting MAPK and NF-κB signaling in a murine model[J]. Int Immunopharmacol,2016,31(2):109-115.