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Solanine induced apoptosis and increased chemosensitivity to Adriamycin in T-cell acute lymphoblastic leukemia cells - PubMed

Solanine induced apoptosis and increased chemosensitivity to Adriamycin in T-cell acute lymphoblastic leukemia cells

Ying-Jie Yi et al. Oncol Lett. 2018 May.

Abstract

Solanine is an alkaloid and is the main extract of the traditional Chinese herb, Solanum nigrum Linn. It has been reported that Solanine has anti-inflammatory and antitumor properties. The present study aimed to investigate the antitumor effect of Solanine in Jurkat cells and demonstrate the molecular mechanism of antitumor activity of Solanine. A Cell Counting Kit-8 assay demonstrated that Solanine inhibited the proliferation of Jurkat cells in a dose-and time-dependent manner. Cell apoptosis was measured by flow cytometry. Flow cytometry revealed that Solanine induced apoptosis in a dose-dependent manner in Jurkat cells. Reverse transcription-quantitative polymerase chain reaction demonstrated that Solanine modulated the mRNA levels of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). Additionally, Bcl-2 and Bax expression was measured using western blot analysis. Western blot analysis revealed a significant increase in the expression of Bax and decrease in the expression of Bcl-2. Solanine increased the chemosensitivity of Jurkat cells to Adriamycin. In summary, the present results indicated that the antitumor activity of Solanine was associated with inhibition of cell proliferation, induction of apoptosis and increasing cytotoxicity of Adriamycin. Therefore, Solanine may have potential as a novel agent for the treatment of acute lymphocytic leukemia.

Keywords: Jurkat cell; Solanine; apoptosis; chemosensitivity.

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Figures

Figure 1.
Figure 1.

Solanine inhibited the proliferation of T-cell acute lymphoblastic leukemia Jurkat cells. Jurkat cells were treated with different concentrations of Solanine (0, 2, 4, 8 and 16 µg/ml) for 24, 48 and 72 h. Growth curves were based on data from Cell Counting Kit-8 assays. Data are expressed as the mean ± standard deviation of triplicate experiments. *P<0.05 vs. 24 h.

Figure 2.
Figure 2.

Solanine induced apoptosis in T-cell acute lymphoblastic leukemia Jurkat cells. Jurkat cells were treated with different concentrations of Solanine (0, 4 and 16 µg/ml) for 24 h. Annexin VFITC/phycoerythirin staining was conducted in order to measure cell apoptosis. Data are expressed as the mean ± standard deviation of triplicate experiments. *P<0.05 vs. 0 µg/ml Solanine. FITC, fluorescein isothiocyanate; PE, phycoerythrin.

Figure 3.
Figure 3.

Effect of Solanine on (A) Bax and (B) Bcl-2 mRNA expression in Jurkat cells. The Jurkat cells were treated with different concentrations of Solanine (0, 4 and 16 µg/ml) for 24 h before Bcl-2 and Bax mRNA levels were determined by reverse transcription-quantitative polymerase chain reaction. Data are expressed as the mean ± standard deviation of triplicate experiments. *P<0.05 vs. vs. 0 µg/ml Solanine. Bcl-2, B-cell lymphoma-2; Bax, Bcl-2-associated X protein.

Figure 4.
Figure 4.

Effect of Solanine treatment on (A) Bax and (B) Bcl-2 expression in T-cell acute lymphoblastic leukemia Jurkat cells. Jurkat cells were treated with Solanine (0, 4 and 16 µg/ml) for 24 h. (C) Protein expression levels of Bcl-2 and Bax were measured by western blot analysis. GAPDH was used as a positive control. Data are expressed as the mean ± standard deviation of triplicate experiments. *P<0.05 vs. 0 µg/ml Solanine. Bcl-2, B-cell lymphoma-2; Bax, Bcl-2-associated X protein.

Figure 5.
Figure 5.

Effect of Solanine on the chemosensitivity of Jurkat cells to Adriamycin. Cell viability was measured by Cell Counting Kit-8 assay subsequent to treatment with Solanine in the presence of Adriamycin (2 µg/ml for 24 h). Data are expressed as the mean ± standard deviation of triplicate experiments. *P<0.05 vs. 0 µg/ml Solanine in the presence of 2 µg/ml Adriamycin.

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