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Anti-Cancer Agents in Medicinal Chemistry 2020-Mar

Urtica dioica Extract Inhibits Cell Proliferation and Induces Apoptosis in HepG2 and HTC116 as Gastrointestinal Cancer Cell Lines.

Зөвхөн бүртгэлтэй хэрэглэгчид л нийтлэл орчуулах боломжтой
Нэвтрэх / Бүртгүүлэх
Холбоосыг санах ойд хадгалдаг
Mostafa Kardan
Alireza Rafiei
Monireh Golpour
Mohammad Ebrahimzadeh
Haleh Akhavan-Niaki
Sadegh Fattahi

Түлхүүр үгс

Хураангуй

Nowadays the use of plant-derived products has been extensively examined in the treatment of many types of gastrointestinal cancer such as hepatocarcinoma and colon cancer. Urtica dioica is a traditional herb that has many pharmacological effects and wildly used as a therapeutic agent in cancer. Herein, we have evaluated the effects of the different concentrations of Methanolic Extract of Urtica dioica (MEUD) on viability, death pattern, and expression of the apoptosis-related gene in normal Human Dermal Fibroblast (HDF), hepatocarcinoma cell lines (HepG2) and colon-cancer cell line (HCT116).A high-performance liquid chromatography method was developed to simultaneously separate 3 phenolic acids in MEUD. HepG2 and HCT116 cell lines as well as HDF normal cell line were cultured in suitable media. After 24 and 48h, cultured cell with different concentrations of MEUD, Cells viability was assessed by MTT assay, and apoptosis was also evaluated at the cellular level by Annexin V/PI flowcytometry analyzing and AO/EB staining. BCL2 and BAX gene expression were assessed by TaqMan real-time PCR assay.MEUD showed antiproliferative effects on HepG2 and HTC116 cells after 48h with an IC50 value of about 410 and 420μg/ml, respectively (P<0.001). Apoptotic cells were observed in HepG2 and HTC116 cells but not in HDF. Furthermore, the increased level of BAX/BCL-2 ratio was observed in HepG2 and HTC116 cells under the treatment of different concentrations of MEUD Conclusions: The MEUD may influence hepatocarcinoma and colon-cancer cell lines at specific doses and change their proliferation rate by changing the expression of BAX and BCL2.

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