The investigation of the antitumoral effect of Cornus mas L in mice with ehrlich solid tumor

Yilmaz S., Alpa S., Gocmcn A. Y., Ulger H., Arslan E., Yay A. H., ...Daha Fazla

Bratislava Medical Journal, cilt.121, sa.1, ss.22-30, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 121 Sayı: 1
  • Basım Tarihi: 2020
  • Doi Numarası: 10.4149/bll_2020_004
  • Dergi Adı: Bratislava Medical Journal
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.22-30
  • Anahtar Kelimeler: Ehrlich solid tumor, Cornus mas L, anti-tumor, AgNOR, TOTAL ANTIOXIDANT CAPACITY, PROTEIN-SYNTHESIS, ASCITES, CANCER, CURCUMIN
  • Erciyes Üniversitesi Adresli: Evet

Özet

© 2020, Comenius University.AIM: Cornus mas L is commonly used due to its anti-inflammatory, anti-carcinogenic and anti-oxidant properties. In the study, the effects of C. mas L extract on a solid tumor were examined in the Ehrlich solid tumor model developed in Balb/C type mice. METHODS: Ehrlich acid tumor (EAT) cells (1x106 EAT cell) from the stock animal were injected subcutaneously (s.c.) through the nape of the mice. Treatment groups of solid tumor-induced animals received 100 mg/kg and 200 mg/kg of C. mas L extract intraperitoneally (i.p.) for 14 days. RESULTS: Tumor volumes and animal weights were found to be statistically significant compared to the control group (p < 0.05). AgNOR staining was performed in tumor tissues. Statistically significant differences were observed between the groups in terms of TAA/NA ratio (p < 0.05). Immunohistochemical and biochemical parameters were also evaluated. An estimation of tumor proliferation of the lung, liver, brain, kidney, testis and tumor antioxidant parameters viz. lipid peroxidation, reduced glutathione (GSH), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) was made. CONCLUSIONS: Our study showed that the anti-tumor effect of C. mas L in assisted tumor development with EAT cells, was mediated by the enhancement of oxidative stress with multiple mechanisms (Tab. 6, Fig. 12, Ref. 38). Text in PDF www.elis.sk.