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Background: Toll-Like Receptors (TLRs) are the cause of phagocytosis activation and destruction of the infection agents. In addition, new evidences support the idea that TLRs play a vital role in starting the acquired immunity reactions.
Methods: In this study, it has been attempted to infect the BALB/c mice with Leishania ajor () and treat them using morphine and imiquimod; then the expressions of ,4 from treated lesion were studied by using Real-Time PCR method. Treatment with morphine 1 , imiquimod 5% and nalmefene 1 began four weeks after the challenge. After treatment period, half of the mice of each group were killed and their lesions were isolated for RNA extraction and making cDNA. For the rest of mice, lesion size was measured weekly.
Results: The results showed increase of expression of gene among all treated groups relative to the control, and the difference was significant (p<0.05). The expression of gene only was reduced in groups under treatment with morphine and morphine plus nalmefene relative to the control group and in the other groups increased. The highest expression of was seen in the group treated by glucantime (p<0.0001).
Conclusion: However, in this study it was found that despite decreasing the size of lesion in all treated groups, expression of in the morphine, nalmefene, morphine plus nalmefene treated groups compared to the control group was decreased. Therefore, morphine may have a different function mechanism in treatment of the Leishmaniasis with the .
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Methods Cell Biol
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School of Global Health, Chinese Centre for Tropical Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
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