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Background & Objective: Diclofenac is a non-steroidal, anti-inflamatory drug that is prescribed as an analgesic. However, there is little known about the effects of diclofenac on the neural cells. In this study, we investigated the effects of diclofenac as sodium salt on the proliferation and differentiation of PC12 cells.

 

Materials & Methods: This expeimental study was done in Kerman neuroscience research center during 2004. The cell proliferation was evaluated by using XTT assay in the both free-serum neurobasal medium supplemented with B27 supplement and DMEM/F12 medium containing 10% FBS. The nerve growth factor(NGF) – induced differentiation was assessed  by measuring the neurite length for each treatment.

 

Results: The drug toxicity was exhibited at the higher concentrations of 310 mM in the supplemented neurobasal medium. The treatment of cells in the DMEM/F12 medium increased their sensitivity to diclofenac, with 40 and 85% growth inhibition at the 155 and 310 mM concentrations, respectively. The different generics of drug exhibited a equal toxic effects on the PC12 cells. The NGF- induced differentiation was not reduced by toxic and subtoxic concentrations of diclofenac.

 

Conclusion: This study indicated that diclofenac may be able to exhibit its neurotoxic effects through growth inhibition, but not differentiation inhibition. B27 supplement has several antioxidant compounds. Therefore, the difference of diclofenac cytotoxic effects in two culture media suggest that drug cytotoxicity may be related to the oxidative stress.

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Background and Objective: Change in the cell surface and extracellular matrix glycoconjugates has been reported in many cancers. Moreover, diagnostic and prognostic importance of these substances and also their roles in therapeutic modalities for cancerous patients has been emphasized. This study was designed to explore the histochemical study of cellular mucopolysaccharides in esophageal and gastric carcinoma and its relation to tumor differentiation. Materials and Methods: In this laboratory study tissue samples of 40 patients with esophageal squamous cell carcinoma and 40 patients with stomach adenocarcinoma in different grades of tumor were selected from pathology department of Emam Reza hospital in Mashhad, Iran. Tissue samples were stained with Alcian Blue (PH 1 and PH 2.5) for Sulfated and Carboxylated mucosubstances respectively, along with positive and negative controls. Results: Normal esophageal epithelium and carcinoma cells of different grades showed negative reactivity but normal and tumoral stromal cells depicted positive staining in both PHs. In PH 1, normal glandular and carcinoma cells of the stomach were negative but in PH 2 glandular cells were positive though carcinoma cells showed weakly staining. Normal and tumoral gastric stromal cells showed positive staining in PH 1 and PH 2.5. Conclusion: It is highly probable that in the process of cancerization of normal esophageal squamous cells, functional changes, from the perspective of producing Carboxylated and Sulfated mucosubstances, do not occur, whereas some changes in glandular cells of stomach which result in diminishing the production of Carboxylated mucosubstances during cancerization process are observable.

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Background and Objective: Thyroid cancer is a common cancer of the endocrine system, and knowing the etiology can be effective in its treating. On the other hand, the FNA technique is not accurate enough, so finding a biomarker for thyroid cancer is of importance. This study was done to evaluate the NKX2-1 gene as indicator of differentiation of papillary thyroid carcinoma (PTC).
Methods: In this case-control study, 17 fresh PTC tissue samples and 20 adjacent-healthy tissues were collected during thyroidectomy in Isfahan, Iran. RNA extraction was followed by cDNA synthesis. The expression of the NKX2-1 gene was performed using specific primers (exon-junction and intron spanning) using the RT-qPCR method.
Results: An examination of the quality and quantity of extracted RNAs showed that they were intact and suitable for making cDNA. Examination of the melting curve showed a specific amplification of the NKX2-1 gene. The difference in expression of the NKX2-1 gene between PTC and healthy-adjacent tissues was 0.947.
Conclusion: No difference in the expression of the NKX2-1 gene between the healthy tissue adjacent to the tumor and the tissue of the PTC tumor indicates that the PTC tumors were differentiated.