Nano silicon dioxide (Nano-SiO 2 ) has a great deal of application in food packaging, as antibacterial food additives, and in drug delivery systems but this nanoparticle, despite its wide range of utilizations, can generate destructive effects on organs such as the liver, lung, and kidney. This study aimed to investigate the toxicological effects of nano-SiO 2 through apoptotic factors. For this purpose, 40 female rats in 4 groups (n = 10) received 300, 600, and 900 mg/kg/day of nano-SiO 2 at 20-30 nm size orally for 20 days.Relative expression of Caspase3, Bcl-2, and BAX genes in kidney and liver evaluated in Real time-PCR.The Results indicated the overexpression of BAX and Caspase3 genes in the liver and kidney in groups receiving 300 and 900 mg/kg/day of nano-SiO 2 . Bcl-2 gene was up-regulated in the liver and kidney at 600 mg/kg/day compared to the control group. Overexpression of the Bcl-2 gene in the kidney in 300 and 900 mg/kg/day recipient groups was observed (p ≤ 0.05). Histopathological examination demonstrated 600 mg/kg/day hyperemia in the kidney and lung. In addition, at 900 mg/kg/d were distinguished scattered necrosis and hyperemia in the liver. The rate of Epithelialization in the lungs increased. Our study revealed that the oral consumption of nano-SiO 2 can cause respiratory toxicity. The nano-SiO 2 at 300 and 900 mg/kg/day can induce more cytotoxicity in the liver and lung after oral exposure. However, cytotoxicity of nano-SiO 2 at 600 mg/kg/day in the kidney and lung was noticed. Hence, The Using of nano-SiO 2 as an additive and food packaging should be more considered due to their deleterious effects.
Cutaneous melanoma (CM) is a highly metastatic cancer whose incidence rate is heightening worldwide. B7H6, as one of the co-stimulatory ligands of the B7 family, is expressed in malignant cells, involved in tumorigenesis. This study aimed to investigate the significance of B7H6 in CM cell chemosensitivity and metastatic ability. A375 CM cells were transfected with B7H6-siRNA and treated with dacarbazine individually or combined. The MTT assay to estimate half-maximal inhibitory concentration of dacarbazine and cell viability, the apoptotic induction using Annexin V/PI, cell cycle progression via flow cytometry, and wound healing assay for determining the migration ability of cells and assessing the clonogenic potential of A375 cells were executed. Functional analyses were performed to evaluate changes in A375 cells. The results illustrated that B7H6 suppression significantly increased the chemosensitivity of A375 cells to dacarbazine. Apoptosis induction by dacarbazine was enhanced after B7H6 knockdown through modulating Caspase-3, Bax, and Bcl-2 mRNA levels. Western blotting indicated enhancement of cleaved caspase-3 protein expression in treatment groups. A375 cells were arrested at the sub-G1 and S phases when using B7H6-siRNA and dacarbazine. B7H6 suppression combined with dacarbazine restrained cell migration through suppression of matrix metalloproteinase (MMP) expression, including MMP2, MMP3, and MMP9. In addition, the clonogenic ability of A375 cells was decreased by downregulating Sox2, Nanog, and CD44 mRNA levels. A visible decrement in STAT3 protein expression was observed in the combination group. Hence, our findings revealed that B7H6 knockdown with dacarbazine could be a promising treatment approach for cutaneous melanoma.
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