Font Size: a A A

Proliferation Cell Nuclear Antigen Expression In The Model Of Epidermal Proliferation In Subacute And Chronic Dermatitis

Posted on:2008-05-01Degree:MasterType:Thesis
Country:ChinaCandidate:Y H ZhuFull Text:PDF
GTID:2144360212483995Subject:Pathology and pathophysiology
Abstract/Summary:PDF Full Text Request
Objective: Epidermal barrier function would adjust the combination of keratinocyte DNA. In acute animal models, the combination of keratinocyte DNA will be increased while the epidermal barrier function degrades and the increasing extent is in direct retio with the degree of the normal barrier function. When the epidermal barrier function is improved, the combination of keratinocyte DNA will be restrained.The main feature of tissue pathology is epidermal over-proliferation and physiology chang is that epidermal barrier function degrades in the model of subacute and chronic dermatitis. At present , there is no study of relationships between epidermal barrier function and epidermal proliferation in model of subacute and chronic dermatitis. In the experiment, we eastablished models by application of 0.5%2,4-dinitro-1-flucrobenzene (DNFB) and 0.01% TPA on mouse backs. Epidermal barrier function was improved by covering with airtight memberance and repeated application of silicon oil on the models . Tissue pathology and expression of proliferation cell nuclear antigen [PCNA (pc10)] are used to assess whether epidermal proliferation was changed or not. Then we can draw a conclusion about whether epidermal barrier function is realated with epidermal proliferation in the model of subacute and chronic dermatitis.Methods: The mouse were devided into there groups at random named with A,B,C .Every group was devided into subgroup named with 1,2,3. So we have 6 groups marked with A1,A2,A3;B1,B2,B3;C1,C2,C3. A-group is alcohol group. B-group is 0.5%2,4-dinito-1-flucrobene (DNFB) group. C-group is TPA group. Subgroup1 is control group. Subgroup2 is airtightmemberance group. Subgroup3 is silicon oil group. In the experiment, the application of 90% alcohol was only taken in A1 group mouse (alcohol-control group). The mouse were covered with airtight memberance after application of 90% alcohol in A2 group (alcohol- airtight memberance group). The mouse were applicated with silicon oil after 90% alcohol in A3 group (alcohol- silicon oil group). The application of 0.5% DNFB was only taken in B1 group mouse(DNFB -control group). The mouse were covered with airtight memberance after application of 0.5% DNFB in B2 group (DNFB - airtight memberance group). The mouse were applicated with silicon oil after 0.5% DNFB in B3 group (DNFB - silicon oil group). The application of 0.01% TPA was only taken in C1 group mouse (TPA -control group). The mouse were covered with airtight memberance after application of 0.01% TPA in C2 group (TPA - airtight memberance group). The mouse were applicated with silicon oil after 0.01% TPA in C3 group(TPA - silicon oil group). After the mouse fur were removed on the belly and back, Only B-group mouse were applicated with 70μl 0.5% DNFB once a day on the first and second day. From the seventh day, all groups were applicated with the right preperation 70μl once two days. In airtight memberance groups, the mouse skin was coverd with airtight memberance after the right preperation was applicated 30 minutes later. In silicon oil group, silicon oil was daubed on the skin after the right preperation was applicated 30 minutes later, twice aday. It took 25 days to mak ethe models. After the models were established, the tissue samples were taken and examined by pathology and immunnohistochemically stained examined with monodonal antibody [PCNA (pc10)] technique. The skin thickness of each sample was examined and the PCNA-positive cells were observed under the same multiple microscope. The average data was calculated and the statistic analysis was achieved.Results: Tissue pathology shows that epidermal tickness did not changed and inflammation cells were not found in dermis. PCNA-positive cells were only expressed on stratum basalum in alcohol groups. Epidermal tickness increased obviously and there were more inflammation cells in dermis on the model of DNFB and TPA .PCNA-positive cells expressed not only on stratum basalum but also on the middle-low stratum spinosum inDNFB and TPA groups and PCNA-positive cells expressed more obviously. That means that epidermal tickness and the level of PCNA expression increased obviously in the model of DNFB and TPA groups than alcohol groups. There were remarkably statistical differences on epidermal tickness and the level of PCNA in the model of DNFB-control and TPA-control group compared with alcoho-control group (P<0.05). So the models of epidermal proliferation in subacute and chronic dermatitis were successed.There were no statistical differences on epidermal tickness and the level of PCNA between the model of DNFB-airtight memberance and DNFB-control group(P>0.05). The same result came out between the model of TPA- airtight memberance and TPA-control group( P>0.05).There were no statistical differences on epidermic tickness and the level of PCNA between the model of silicon oil and control groups in DNFB and TPA (P>0.05).Conclusion: 1. Repeated application of 0.5% DNFB and 0.01%TPA on the mouse back can make copies of the models of epidermal proliferation in subacute and chronic dermatitis. 2. The level of PCNA expression was increased obviously in the model of subacute and chronic dermatitis. 3. Covering with airtight memberance and application of silicon oil on mouse backs can not effectively adjust the epidermal proliferation in the model of subacute and chronic dermatitis.
Keywords/Search Tags:Proliferation cell nuclear antigen (PCNA), Barrier function, Subacute, Chronic, Proliferation
PDF Full Text Request
Related items