ABSTRACT
Background: osteoarthritis [OA] is a progressive, age-associated disease that is characterized with cartilage destruction, subchondral bone remodeling and inflammation of the synovial membrane. Considering the complications of common treatments of OA, including non-steroidal anti-inflammatory drug [NSAIDs] and corticosteroids, investigating new treatments for this disorder is crucial. Recently, the role of matrix metalloproteinases [MMPs] expression in pathogenesis of OA has attracted attention
Objective: this study aimed to explore the effect of punicic acid [PA] in inhibition of MMPs gene expression in LPS-stimulated Bovine Fibroblast-like synoviocytes [BFLS] as a model of OA
Methods: in the first stage, the toxicity of PA was measured using MTT assay on BFLS cells. Afterward, the cells were stimulated by LPS [Lipopolysaccharide] and MMPs [Matrix Metalloproteinase] expression level in the BFLS cells were investigated using Real-Time PCR, in vitro Migration and Gelatin Zymography, Western Blot Analysis, ELISA Assay and Invasion Assay
Results: the results showed that PA significantly decreased MMP-9 expression levels in LPS stimulated BFLS cells; also, it suppressed migration and invasion of the mentioned cells. However, PA had no significant effect on MMP-1-2-3
Conclusion: based on our results PA could significantly reduce the activity and inflammatory effect of MMP-9 in OA, its potential role as a supplementary agent to common NSAIDs and corticosteroids was confirmed. Nonetheless, cellular modeling does not significantly confirm the beneficial effect of OA in patients
ABSTRACT
Despite improvements in the diagnosis and treatment of lung cancer in the past two decades, it has remained the most common cause of death from cancer worldwide. Among all genes that are mutated in lung cancer, TP[53] located on chromosome 17[P]13/1 has a significant diagnostic and prognostic value. TP[53] mutations have been extensively studied in lung cancer and TP[53] mutational spectra have been used for finding the origin[s] and mechanisms of these mutations in lung cancer development. The present study was conducted to investigate the TP[53] mutations in patients with Non- small cell lung cancer hospitalized during 1997-2005 in Afzalipour Hospital, Kerman, Iran. Formalin- fixed, Paraffin- embedded tissues from lung cancer patients undergone surgery between 1997 to 2005 were evaluated. The mutational status of the TP[53] gene [exons 5 and 8] was screened by polymerase chain reaction [PCR] analysis followed by sequencing. Of all cases of squamous cell carcinoma, 73 mutations were found in Exon 5 [in 18 cases] and 47 mutations in Exon 8 of TP[53] gene [in 15 cases]. we identified mutation hot spot at codons 6, 14, 25 of exon 5 and codons 2, 27, 35 of exon 8 of TP[53] gene. Tansversions [G to T, A to T and G to C] and deletion mutations were the most in both exons 5 and 8. The incidence of G to T transversion mutations did not significantly differ between Exons 5 and 8. Higher prevalence of mutations in TP53 gene in the present study comparing to previous studies may be due to genetic, environmental and some epidemiological factors such as diet and life style of studied subjects