本文選題：等離子體 + 口腔潰瘍��； 參考：《重慶醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:本實(shí)驗(yàn)擬通過建立口腔潰瘍動(dòng)物模型,觀察低溫常壓等離子體對金黃地鼠實(shí)驗(yàn)性頰囊黏膜潰瘍愈合時(shí)間及潰瘍組織中超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量的影響。探討低溫常壓等離子體用于口腔潰瘍局部治療的可行性,為可能的臨床應(yīng)用提供參考依據(jù)。材料與方法:1.利用氧自由基誘導(dǎo)法建立金黃地鼠口腔潰瘍模型,潰瘍形成后,觀察潰瘍形態(tài)及大小,作病理切片觀察判斷建模是否成功。2.56只動(dòng)物隨機(jī)分為:第1批建模組(n=48)、第2批建模組(即潰瘍模型組,n=4,于第1批動(dòng)物建模72 h后建模)及正常對照組(n=4,正常飼養(yǎng),不做任何處理)。其中,第1批建模組又隨機(jī)均分為:潰瘍自然愈合組、藥物組、2個(gè)單純通氣組(30 s、120 s組)及2個(gè)等離體處理組(30 s、120 s組),每組8只。第1批建模動(dòng)物潰瘍形成后,記錄潰瘍形態(tài)及大小,進(jìn)行相應(yīng)實(shí)驗(yàn)處理,每天1次,持續(xù)3天。末次治療結(jié)束24 h后即第2批動(dòng)物建模72 h后,每組隨機(jī)選取4只動(dòng)物測定頰囊黏膜潰瘍組織中S0D活力及MDA含量;觀察剩余24只動(dòng)物各組潰瘍的愈合時(shí)間,待潰瘍完全愈合后檢測相應(yīng)部位黏膜組織中S0D活力及MDA含量。結(jié)果:1.該方法建模72小時(shí)后觀察到黏膜潰瘍形成,潰瘍?yōu)閳A形或類圓形,直徑約0.5-0.6cm,表面淡黃色假膜覆蓋,周圍可有充血、水腫,鏡下病理特點(diǎn)與人的口腔潰瘍相似。2.(1)潰瘍平均面積(0.216±0.014)cm2,各組間潰瘍面積相比無顯著差異(P0.05);等離子體組愈合時(shí)間明顯短于其余各組,30、120 s兩個(gè)等離子體組潰瘍愈合時(shí)間相比無顯著差異(P0.05)。(2)與正常對照組相比,建模成功后的潰瘍模型組頰囊黏膜組織中SOD活性顯著降低(P=0.00),MDA含量顯著增高(P=0.00)。末次處理24 h后,等離子體組SOD活性和MDA含量與正常對照組沒有顯著差異(P0.05),但與潰瘍模型組及其余各組相比均有顯著差異(P=0.00);而30s、120s兩個(gè)等離子體組間沒有顯著差異(P0.05)。(3)潰瘍完全愈合后各實(shí)驗(yàn)組囊黏膜組織中SOD活性和MDA含量之間及其與正常對照組間差異沒有顯著性。結(jié)論:1.實(shí)驗(yàn)結(jié)果顯示:以氧自由基誘導(dǎo)法成功建立口腔潰瘍動(dòng)物模型,所得潰瘍臨床與病理表現(xiàn)與人類口腔潰瘍相似。2.實(shí)驗(yàn)結(jié)果顯示:(1)該方法建模,形成的潰瘍大小無顯著區(qū)別;(2)該方法建模后潰瘍形成時(shí),黏膜組織中SOD活性明顯降低,MDA含量明顯增高。30 s、120s等離子體處理,可使甲基紫晶所致金黃地鼠頰囊黏膜潰瘍組織中SOD活性及MDA含量較快回復(fù)到正常水平,明顯縮短潰瘍愈合時(shí)間。(3)以該方法建立口腔潰瘍動(dòng)物模型,待潰瘍完全愈合后,頰囊粘膜組織中SOD、MDA均能回復(fù)到正常水平。
[Abstract]:Aim: to establish an animal model of oral ulcer and to observe the effects of plasma at low temperature and atmospheric pressure on healing time of experimental cheek pouch ulcer and the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) of malondialdehyde (MDA) in experimental cheek pouch mucosa of golden hamsters.To explore the feasibility of hypothermia and atmospheric pressure plasma in the local treatment of oral ulcer, and to provide reference for the possible clinical application.Materials and methods: 1.The oral ulcer model of golden hamsters was established by oxygen free radical induction. After the ulcers were formed, the morphology and size of the ulcers were observed.Pathological sections were made to determine whether the model was successful or not. 2.56 animals were randomly divided into three groups: the first group, the first group, the second group, the ulcer model group, the second group (namely, the ulcer model group, for 72 hours after modeling) and the normal control group, the control group, the control group, for normal feeding.Don't do anything.Among them, the first group was randomly divided into three groups: spontaneous ulcer healing group, drug group, two simple ventilation group (30 s / 120 s) and two iso-isolated treatment groups (30 s / 120 s) with 8 rats in each group.After the ulcer was formed in the first batch of model animals, the ulceration morphology and size were recorded, and the corresponding experimental treatment was carried out once a day for 3 days.24 hours after the end of the last treatment, 72 hours after the second batch of animal models, 4 animals in each group were randomly selected to determine the activity of S0D and the content of MDA in the tissues of buccal pouch mucosa ulcer, and the healing time of ulcer in each group of the remaining 24 animals was observed.The activity of S0D and the content of MDA in mucosal tissue were detected after the ulcer healed completely.The result is 1: 1.The formation of mucous ulcer was observed 72 hours after modeling. The ulcer was round or round in diameter, about 0.5-0.6 cm in diameter. The surface was covered with yellowish pseudomembrane, and there could be congestion and edema around it.The average area of ulcer was 0.216 鹵0.014 路cm ~ (2) and there was no significant difference in ulcer area between each group (P < 0.05), and the healing time of plasma group was significantly shorter than that of other groups (30120 s and 30120 s).There was no significant difference between the two groups.The activity of SOD in the buccal pouch mucosa of the ulcer model group was significantly decreased after the establishment of the model.After the last treatment for 24 hours,There was no significant difference in SOD activity and MDA content between the plasma group and the normal control group, but there was significant difference between the plasma group and the ulcer model group and other groups, but there was no significant difference between the two plasma groups in 30 s ~ 120 s.There was no significant difference in SOD activity and MDA content between the experimental group and the normal control group.Conclusion 1.The experimental results showed that the animal model of oral ulcer was successfully established by oxygen free radical induction, and the clinical and pathological manifestations of the ulcer were similar to those of human oral ulcer.The experimental results showed that the SOD activity in mucosal tissue decreased significantly when the ulceration was formed by the method, and the content of MDA in the mucosal tissue increased significantly after the ulcer was formed by the method, and the plasma treatment showed that the content of SOD in the mucosal tissue was significantly increased by plasma treatment for .30 sg / 120 s.The activity of SOD and the content of MDA in golden hamster cheek pouch mucosa ulcer tissue induced by methyl amethyst were quickly returned to normal level, and the healing time of ulcer was shortened obviously.) the animal model of oral ulcer was established by this method, and after the ulcer was completely healed, the animal model of oral ulcer was established.MDA in cheek pouch mucosa could return to normal level.
【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R781.5

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