Layasadat Khorsandi , Mahmood Orazizadeh ,
Volume 14, Issue 5 (2-2013)
Abstract
Background : Previous studies have demonstrated that Dexamethasone, a widely used GC, induces apoptosis in testis by decreasing the testosterone levels. Galectin-3 (Gal-3), a member of the ß-galactoside-binding lectins, plays critical roles in diverse biological events including cell growth, apoptosis, cell adhesion and immunomodulation. In this study, the effects of Dexamethasone (Dex) on galectin-3 (Gal-3) expression in the mouse testicular tissue were investigated.
Materials and Methods: Sixteen male NMRI (6-8 weeks old) randomly divided into two groups. Experimental group received 7 mg/kg Dex for 7 days by intrapritoneal injection. Control group received normal saline for 7 days by intrapritoneal injection.One day after the last injection the mice were sacrificed and the samples were collected (from adult NMRI mice), fixed in 10% buffered formalin and embedded in paraffin for immunohistochemistry and TUNEL studies. HSCORE was used for scaling and comparison of results.
Results: In the control group, seminiferous tubules showed positive immunoreactivity to Gal-3 at all stages. In particular, stages of VII-VIII showed the most immunoreactivity. The expression pattern of Bcl-2 and Galectin-3 was similar in both control and experimental groups.
HSCORE assessments showed a significant decrease in expression of Gal-3 at all stages of spermatogenic cycle in Dex treated mice (P<0.001). ). Apoptotic index (AI) showed a significant increase at all stages of spermatogenesis cycle in the experimental group (P<0.01)
Conclusion: Reduction in expression of Gal-3 in seminiferous tubules in Dex treated mice indicates that it probably involves in testicular germ cell apoptosis.
Firoozeh Niazvand, Laya Sadat Khorsandi, Forouzan Absalan, Atefeh Ashtari,
Volume 22, Issue 2 (8-2020)
Abstract
Background: Due to proven anti-tumor activity of quercetin (QT), however the low effectiveness of QT has restricted its use. This study aimed to assess the toxic effect of QT encapsulated in solid lipid nanoparticles (QT-SLNs) on the cell death (Autophagy) of MCF-7 human breast cancer cells.
Materials and Methods: MCF-7 and MCF-10A (non-tumorigenic cell line) cell lines treated with 25 µml/mL of QT or QT-SLNs for 48 h. Cell viability and Autophagy were evaluated to determine the toxic effectiveness of the QT-SLNs.
Results: The QT-SLNs with appropriate characteristics were prepared. The QT-SLNs showed sustained QT release until 48 h. Cytotoxicity assessments indicated that QT-SLNs inhibited MCF-7 cells growth with a low IC50 (50% inhibitory concentration) value, compared to the free QT. QT-SLNs induced a significantly increased in Autophagy in the MCF-7 cells. Following QT-SLNs treatment, the expression of the ATG-5 protein significantly increased in comparison with free QT-treated cells. Furthermore, The QT-SLNs significantly increased autophagy indexes in MCF-7 cells. Viability and autophagy of MCF-10A cells were not affected by QT or QT-SLNs.
Conclusions: According to these results, SLN significantly enhanced the toxic effect of QT against human breast cancer cells.
