發(fā)布時間：2019-06-25 19:42

【摘要】：背景:口腔潰瘍是口腔科中最常見、且頻繁發(fā)作的疾病。因?yàn)槠洳∫虿C(jī)尚未完全明確,當(dāng)今醫(yī)學(xué)對其尚無確切的治療方法及特效藥物。中醫(yī)主張辯證論治和治病求本,因此中醫(yī)藥治療口腔潰瘍具有一定的優(yōu)勢。中藥復(fù)方口瘍康臨床應(yīng)用治療陰虛火旺所導(dǎo)致的口腔炎癥療效顯著。目的:通過建立陰虛型口腔潰瘍大鼠模型,來評價口瘍康的治療作用,并從p38MAPK和ERK1/2信號通路方面探討其作用機(jī)制,為口瘍康的研究開發(fā)提供實(shí)驗(yàn)依據(jù)。方法:1、將20只SD大鼠隨機(jī)分為2組,每組10只。模型組大鼠灌胃甲狀腺片混懸液,給藥21日;空白組大鼠灌胃0.9%的氯化鈉溶液。第22日,模型組大鼠麻醉后,用鑷子夾取直徑約5mm的濾紙片在56%氫氧化鈉溶液中浸泡過后,置于大鼠一側(cè)頰黏膜處燒灼20 s;空白組大鼠不作處理。24h后觀察潰瘍形成情況,檢測大鼠血清中cAMP、cGMP水平及紅細(xì)胞膜Na+-K+-ATP酶活性。2、將72只SD大鼠隨機(jī)分為6組,分別為空白組、模型組、知柏地黃丸組及口瘍康高、中、低劑量組,每組12只。建立陰虛型口腔潰瘍大鼠模型,評價口瘍康的治療作用,檢測大鼠血清中cAMP、cGMP水平及紅細(xì)胞膜Na+-K+-ATP酶的活力值,潰瘍黏膜組織中TNF-α、IL-6、IL-10、EGF、TGF-β1水平及p38MAPK、ERK1/2蛋白磷酸化水平。結(jié)果:1、與空白組比較,模型組大鼠口腔黏膜形成直徑5mm左右的潰瘍,且出現(xiàn)體重逐漸減輕,飲水量及體溫逐漸增加,舌偏紅,煩躁多動等類似陰虛癥狀;血清cAMP水平明顯升高,cGMP水平明顯降低,紅細(xì)胞膜Na+-K+-ATP酶活性明顯升高(P0.01);顯微鏡下觀察模型組大鼠口腔黏膜上皮層細(xì)胞溶解壞死并脫落,黏膜固有層下有許多炎癥細(xì)胞浸潤,以淋巴細(xì)胞和中性粒細(xì)胞為主,并可見血管內(nèi)皮細(xì)胞壞死,纖維素性滲出,形成大量壞死組織。2、與空白組比較,模型組大鼠口腔黏膜形成潰瘍,且出現(xiàn)類似陰虛的癥狀;cAMP、TNF-α、IL-6水平、Na+-K+-ATP酶的活力及p38MAPK、ERK1/2蛋白磷酸化水平明顯升高,cGMP、IL-10、EGF、TGF-β1水平明顯降低(P0.05,P0.01)。與模型組比較,口瘍康各劑量組和知柏地黃丸組大鼠陰虛癥狀明顯改善,潰瘍愈合時間明顯縮短;cAMP、TNF-α、IL-6水平、Na+-K+-ATP酶的活力及p38MAPK、ERK1/2蛋白磷酸化水平明顯降低,cGMP、IL-10、EGF、TGF-β1水平明顯升高(P0.05,P0.01)。結(jié)論:1、本研究成功建立了陰虛型口腔潰瘍大鼠模型,該模型實(shí)施簡便可行、容易重復(fù)。2、口瘍康對陰虛型口腔潰瘍模型大鼠有明顯的治療作用,其機(jī)制可能是通過調(diào)節(jié)機(jī)體代謝、相關(guān)細(xì)胞因子水平及p38MAPK和ERK1/2蛋白磷酸化水平實(shí)現(xiàn)的。
[Abstract]:Background: oral ulcer is the most common and frequent disease in stomatology. Because its etiology and pathogenesis are not completely clear, there is no exact treatment and special drugs in today's medicine. Traditional Chinese medicine advocates dialectical treatment and treatment of diseases, so traditional Chinese medicine has certain advantages in the treatment of oral ulcer. The clinical application of traditional Chinese medicine compound Kou Yang Kang is effective in the treatment of oral inflammation caused by deficiency of yin and fire. Objective: to evaluate the therapeutic effect of Kou Yangkang by establishing a rat model of oral ulcer with yin deficiency type, and to explore its mechanism from the aspects of p38MAPK and ERK1/2 signal pathway, so as to provide experimental basis for the research and development of Kou Yangkang. Methods: 1. 20 SD rats were randomly divided into two groups with 10 rats in each group. The rats in the model group were given the suspension of thyroid tablets for 21 days, and the rats in the blank group were given 0.9% sodium chloride solution. On the 22nd day, after anaesthesia, the filter paper about 5mm was clipped with tweezers and soaked in 56% sodium hydroxide solution, and then burned in the buccal mucosa of rats for 20 s. The rats in the blank group were not treated. 24 hours later, the formation of ulcer was observed, and the level of cAMP,cGMP in serum and the activity of Na-K-ATP enzyme in erythrocyte membrane were measured. 2. 72 SD rats were randomly divided into 6 groups: blank group, model group, Zhibai Dihuang pill group and Kou Yang Kang Gao, medium and low dose groups with 12 rats in each group. The rat model of oral ulcer with yin deficiency was established to evaluate the therapeutic effect of Kou Yangkang. The levels of cAMP,cGMP in serum, the activity of Na-K-ATP enzyme in erythrocyte membrane, the levels of TNF- 偽, IL-6,IL-10,EGF,TGF- 尾 1 in ulcer mucosa and the phosphorylation of p38MapK and ERK1 鈮，

本文編號：2505952