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1.
Tianjin Medical Journal ; (12): 1099-1102, 2013.
Article in Chinese | WPRIM | ID: wpr-474674

ABSTRACT

Objective To investigate the effects of all-trans retinoic acid (ATRA)-intragastric-administration on the survival time of mouse skin allografts and the role of interleukin (IL)-23 and IL-17 thereof. Methods The skin trans-plantation of mice was done by DBA/2 as donors and Balb/c as recipients. The recipients were divided randomly into three groups:control group, low-dose group and high-dose group. Mice of the corresponding groups were intragastrically adminis-tered corn oil, 10 mg/kg ATRA and 30 mg/kg ATRA respectively from 1 day before the transplantation to the 14th day after the transplantation. The survival time of transplanted skin was observed after the operations. Skin grafts of mice were harvested for histopathological examination in three groups. The serum levels of IL-23 and IL-17 were measured by enzyme-linked im-munosorbent assay (ELISA). The expression levels of IL-23, RORγt and IL-17 mRNA in skin allografts were detected by re-al-time fluorescent quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Results Compared with con-trol group, the average survival time of mouse skin allografts was significantly prolonged in low-dose group and high-dose group (P<0.05). The less lymphocyte infiltration and destruction of architecture were found in the skin biopsies. The serum expression of IL-23 protein was lower (P<0.05), but no significant difference was found in two treatment groups. The serum expression levels of IL-17 protein were reduced in turn in receptors of control group, low-dose group and high-dose group (P < 0.05). The expression levels of IL-23, RORγt and IL-17 mRNA in skin grafts were significantly lower in low-dose group and high-dose group than those of control group (P<0.05), but no significant difference was found in two treatment groups. Conclusion ATRA can effectively prolong the survival time of skin allografts, which may related with the inhibi-tion of the expression of IL-23, RORγt and IL-17 mRNA and the development of IL-23 and IL-17 protein.

2.
Chinese Journal of Rheumatology ; (12): 538-541, 2009.
Article in Chinese | WPRIM | ID: wpr-393557

ABSTRACT

Objective The therapeutic effect of epigallocatechin-3-gallate (EGCG) on the collageninduced arthritis model (CIA) was observed and its immunological mechanism was analyzed. Methods EGCG was administered to CIA mice and PBS was admitted as negative control. The severity of CIA was evaluated by clinical scores and histopathological assessment (H-E staining). Immunological mechanisms inv-suppressive effect on IL-17 secretion of CD4+T cells (EGCG group: 0.41%; PBS group: 4.05% ) and inhibitive activity of C Ⅱ -reactive splenocytes proliferation. There was statistical significant difference between IKB expression and down-regulate phosphorylated IKB expression in lymph node cells of CIA mice.Conclusion EGCG can significantly ameliorate the severity of CIA. The therapeutic mechanisms may be related to inhibition of C Ⅱ -reactive splenocyte proliferation and IL-17 secretion and via inhibiting the activity of NF-κB by inducing the expression of IKB and by suppressing the expression of phosphorylated IKB in CIA mice.

3.
Journal of Third Military Medical University ; (24)1988.
Article in Chinese | WPRIM | ID: wpr-551297

ABSTRACT

An inbred strain of DXB/c mouse has been established by hybridization between DBA/2 female mice and C57BL/6 male ones and subsequently by sibmating their offsprings beginning from the F2 generation.Now DXB/c mouse has been passed for 28 generations of full sibmating since 1979.Genetic checkup by means of skin grafting,mandibular morphology analysis,mixed lymphocyte cultivation,coat colour gene testing,and biochemical marker gene examination confirmed that the full homozygosity of alleles has been achieved in DXB/c mouse and DXB/c mouse comforms to the criteria of an inbred strain of mouse.In addition,the genetic background of DXB/c mouse is composed of the genes of its progenitors DBA/2 and C57BL/6 as shown by coat colour gene testing and biochemical marker gene examination.

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