本文選題：電離輻射 + 頜下腺�。� 參考：《廣西醫(yī)科大學(xué)》2012年博士論文

【摘要】：目的：放射治療是鼻咽癌等頭頸部惡性腫瘤的主要治療手段。鼻咽癌等頭頸部惡性腫瘤患者放射治療的常規(guī)照射野以兩側(cè)對(duì)穿外照射為主,涎腺特別是腮腺位于放療靶區(qū)內(nèi),輻射造成涎腺組織損傷,引起腺體功能障礙,唾液分泌減少,放療后患者發(fā)生口腔干燥癥,嚴(yán)重影響生活質(zhì)量。目前對(duì)輻射導(dǎo)致的口干癥仍以綜合對(duì)癥治療,缺乏有效防治的措施。研究涎腺輻射誘導(dǎo)的損傷機(jī)制,尋找既能對(duì)抗輻射又能抑制腫瘤的藥物,對(duì)疾病的治療有重要的臨床意義。本研究通過(guò)脫氧核苷酸末端轉(zhuǎn)移酶介導(dǎo)的dTP缺口末端標(biāo)記(TdT-mediated dUTP nick end labeling, TUNEL)、電鏡病理形態(tài)學(xué)、免疫組織化學(xué)染色、細(xì)胞培養(yǎng)、細(xì)胞毒性試驗(yàn)(MTT法)、裸鼠移植瘤模型、逆轉(zhuǎn)錄聚合酶鏈?zhǔn)椒磻?yīng)(reverse transcription polymerase chain reaction, RT-PCR)等檢測(cè)技術(shù),旨在了解不同輻射劑量對(duì)大鼠頜下腺輻射誘導(dǎo)損傷的早期(1-3天)情況,在確定輻射誘導(dǎo)涎腺損傷的干預(yù)輻射劑量及探討損傷機(jī)制后,予以LJP藥物干預(yù)以及觀察其對(duì)頜下腺輻射損傷是否具有防護(hù)作用,再觀察LJP對(duì)人鼻咽癌HONE1和CNE2細(xì)胞增殖以及人鼻咽癌HONE1裸鼠移植瘤是否有影響,探討LJP抗人鼻咽癌細(xì)胞的機(jī)制,為L(zhǎng)JP的涎腺防輻射和抗鼻咽癌提供實(shí)驗(yàn)依據(jù)。 方法：本研究分三部分：第一部分,不同劑量60Co Y射線照射對(duì)大鼠頜下腺凋亡相關(guān)因子表達(dá)及形態(tài)學(xué)的影響；第二部分,海帶多糖對(duì)頜下腺60Co Y射線誘導(dǎo)損傷的防護(hù)作用；第三部分,海帶多糖對(duì)人鼻咽癌細(xì)胞株裸鼠移植瘤的抑制作用。第一部分實(shí)驗(yàn)方法：將48只Wistar大鼠隨機(jī)分組原則分為：(1)正常對(duì)照組(n=12)；(2)放療7.5Gy組(n=12)；(3)放療15Gy組(n=12)；(4)放療22.5Gy組(n=12)。放療組予以每只一次性總劑量15Gy的γ-ray照射,而對(duì)照組未予照射。于放療后1 d、3 d,取各組6只大鼠頜下腺組織固定后冷凍切片,免疫組織化學(xué)SP法檢測(cè)P53,Caspase-3表達(dá)情況以及TUNEL法檢測(cè)細(xì)胞凋亡。每組隨機(jī)取1只頜下腺掃描電鏡(Transmission electron microscope,SEM)檢查,觀察頜下腺的形態(tài)學(xué)病理變化。第二部分實(shí)驗(yàn)方法：24只Wistar大鼠隨機(jī)分組原則分為：(1)正常對(duì)照組(n=6)；(2)LJP高劑量放療組(300mg/kg/只/天的LJP)(n=6)；(3)LJP低劑量放療組(30m/kg/只/天的LJP)(n=6)。(4)放療對(duì)照組(n=6)。于放療前3 d、后3 d之間予以上述藥物腹腔注射；放療組以每只一次性總劑量15Gy的γ-ray照射,而對(duì)照組未予照射。各組6只在放療后第3天上午活體各取大鼠雙頜下腺組織,固定后冷凍切片,免疫組織化學(xué)SP法檢測(cè)P53, Caspase-3表達(dá)情況以及TUNEL法檢測(cè)細(xì)胞凋亡。15只Wistar大鼠作電鏡觀察,分成7.5Gy、15Gy、22.5 Gy三個(gè)劑量組①正常對(duì)照組(n=1)；②LJP高劑量放療組(n=1)；③LJP低劑量放療組(n=1)；④放療對(duì)照組(n=1)；⑤蔗糖陰性對(duì)照組(n=1),同上述方法給藥,在放療后第3天上午活體取大鼠頜下腺組織電鏡檢查,觀察頜下腺的形態(tài)學(xué)病理變化。第三部分實(shí)驗(yàn)方法：應(yīng)用MTT法檢測(cè)LJP對(duì)人NPC細(xì)胞株(HONE1和CNE2)增殖的抑制作用。30只雄性裸鼠隨機(jī)分為組：①NS(正常對(duì)照組：NSO. lml/lOg/d) (n=6);②LJP 12.5 (LJP12.5mg/kg/d) (n=6);③LJP 25(LJP25mg/kg/d) (n=6);④LJP50 (LJP50mg/kg/d) (n=6);⑤DDP(陽(yáng)性對(duì)照組：DDP 2 mg/kg/d) (n=6)。以人NPC細(xì)胞株HONE1建立裸鼠皮下移植瘤模型,以分組的藥物進(jìn)行體內(nèi)抑瘤實(shí)驗(yàn),計(jì)算抑瘤率,RT-PCR檢測(cè)移植瘤凋亡相關(guān)基因Bax、Bcl-2、Caspase-3,8,9信使核糖核酸(messenger RNA, mRNA)的表達(dá)。 結(jié)果：第一部分：①p53的表達(dá)為：7.5 Gvld、3d照射組與對(duì)照組差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05)；15 Gy1d、3d照射組與對(duì)照組比較差異有顯著性統(tǒng)計(jì)學(xué)意義(p0.01),22.5Gy3d照射組與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；15 Gy照射組1d和3d間的比較差異有顯著性統(tǒng)計(jì)學(xué)意義(p0.01),7.5 Gy、22.5 Gy照射組1 d與3d間的比較差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05)。②Caspase-3表達(dá)為：7.5 Gy、22.5 Gy照射組1 d和3d、15 Gy照射組3d與對(duì)照組比較差異有顯著性統(tǒng)計(jì)學(xué)意義(p0.01)；15 Gy照射組1d與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)。15 Gy照射組1d與3d間的比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；7.5 Gy、22.5 Gy照射組1 d與3d間的比較差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05)。③tunel染色表達(dá)為：7.5 Gy照射組3d和正常組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；15 Gy照射組1d、22.5 Gy照射組1d、3d與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；15 Gy照射組3d與對(duì)照組比較差異有顯著統(tǒng)計(jì)學(xué)意義(p0.01)；7.5 G、15 Gy、22.5 Gy照射組1 d與3d比較差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05)；7.5 G、15 Gy、22.5 Gy照射組組間比較差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05)。④電鏡觀察結(jié)果：7.5Gy放療組漿液性腺泡細(xì)胞及導(dǎo)管細(xì)胞,核膜完整,核仁消失,核內(nèi)異染色質(zhì)凝集成塊狀并邊集于核膜內(nèi)側(cè),胞質(zhì)內(nèi)粗面內(nèi)質(zhì)網(wǎng)輕度擴(kuò)張,線粒體稍腫脹,嵴模糊不清。導(dǎo)管細(xì)胞,可見細(xì)胞膜皺縮,胞質(zhì)內(nèi)線粒體腫脹,嵴斷裂、減少或消失,胞核完整,核仁清晰。15Gy放療組漿液性腺泡細(xì)胞及導(dǎo)管細(xì)胞,細(xì)胞皺縮,電子密度增高,核膜完整,核仁消失,核內(nèi)異染色質(zhì)明顯增多、凝集成塊狀并邊集于核膜內(nèi)側(cè)；粗面內(nèi)質(zhì)網(wǎng)明顯減少并擴(kuò)張,分泌顆粒亦減少明顯,且顆粒內(nèi)排列紊亂,線粒體結(jié)構(gòu)模糊不清。22.5Gy放療組漿液性腺泡細(xì)胞及導(dǎo)管細(xì)胞,細(xì)胞皺縮,電子密度增高,核膜不完整,核內(nèi)異染色質(zhì)凝集成塊狀并邊集于核膜內(nèi)側(cè),核周隙增寬；胞質(zhì)內(nèi)粗面內(nèi)質(zhì)網(wǎng)大量減少,并擴(kuò)張明顯,結(jié)構(gòu)紊亂,分泌顆粒消失,殘余少量線粒體,核內(nèi)異染色質(zhì)開始增多。第二部分：①p53的表達(dá)為：放療組與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；放療組組內(nèi)比較差異有統(tǒng)計(jì)學(xué)意義(p0.05),高劑量LJP組的細(xì)胞凋亡值最低。②Caspase-3表達(dá)結(jié)果為：放療組與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；LJP30組與LJP300組比較差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05),LJP30組、LJP300組與放療組比較減少差異有統(tǒng)計(jì)學(xué)意義(p0.05)。③TUNEL染色結(jié)果為：LJP30、LJP300組與放療組相比差異有統(tǒng)計(jì)學(xué)意義(p0.05)；LJP30組與LJP300組比較差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05)。④電鏡觀察結(jié)果：7.5 Gy、15 Gy、22.5 Gy三組的細(xì)胞核、線粒體、內(nèi)質(zhì)網(wǎng)以及分泌泡等結(jié)構(gòu)隨著劑量的增加,呈現(xiàn)損傷加重的特征,LJP30. LJP300組細(xì)胞與放療對(duì)照、蔗糖對(duì)照組比較,細(xì)胞結(jié)構(gòu)損傷較輕,對(duì)細(xì)胞有保護(hù)作用。第三部分：①M(fèi)TT結(jié)果：LJP對(duì)HONE1細(xì)胞的IC10為76.85μg/ml, IC20為115.31μg/ml, IC30為153.77μg/ml; LJP對(duì)CNE2細(xì)胞的IC10為18.92μg/ml, IC20為57.38μg/ml, IC30為98.85μg/ml。LJP對(duì)HONE1細(xì)胞、CNE2細(xì)胞工C5。濃度分別為240μg/ml、180μg/ml。②裸鼠移植瘤的干預(yù)結(jié)果：DDP組的平均抑瘤率為63.5%(與NS組比較,p0.01),12.5mg/kg LJP組對(duì)移植瘤的平均抑瘤率僅為16.4%(與NS組比較,p0.05),抑制效果不明顯,而25mg/kg和50mg/kg LJP組對(duì)移植瘤的平均抑瘤率分別為33.7%(與NS組比較,p0.05)和47.0%(與NS組比較,p0.01)。③RT-PCR:LJP12.5、LJP25、LJP50、DDP2組的Bax mRNA表達(dá)與對(duì)照組NS比較差異有統(tǒng)計(jì)學(xué)意義(p0.05); LJP12.5、LJP25、LJP50、DDP2組的Bcl-2 mRNA表達(dá)與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05); LJP 12.5、LJP 25、LJP 50、DDP2組的Bax/Bcl-2比值與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；Bax mRNA表達(dá)：LJP25 LJP50 LJP12.5DDP2,組間的比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；Bcl-2mRNA表達(dá)：LJP25/LJP12.5LJP 50DDP2,組間的比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)。LJP 12.5、LJP 25、LJP 50、DDP2組Caspase-3、Caspase-9 mRNA表達(dá)與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05); LJP25、LJP50、DDP2組Caspase-8 mRNA表達(dá)與對(duì)照組比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)。Caspase-3 mRNA表達(dá)：DDP2 LJP 50 LJP 25 LJP 12.5,各組之間表達(dá)比較差異有統(tǒng)計(jì)學(xué)意義(p0.05)；Caspase-8 mRNA表達(dá)：NS組和LJP12.5組無(wú)差異,LJP25、LJP 50表達(dá)無(wú)差異,LJP 25、DDP2表達(dá)無(wú)差異；Caspase-9mRNA表達(dá)：LJP 12.5、LJP 25、LJP 50表達(dá)均無(wú)差異,且均低于DDP2處理組的表達(dá)。 結(jié)論： 1.60Coγ射線照射可引起大鼠頜下腺早期細(xì)胞凋亡。 2.60Coγ射線(7.5Gy、15 Gy、22.5 Gy)照射誘導(dǎo)的頜下腺細(xì)胞凋亡有劑量-效應(yīng)關(guān)系。 3.15 Gy照射劑量誘導(dǎo)的頜下腺細(xì)胞損傷在早期(1-3天)處于修復(fù)和凋亡的變動(dòng)階段。 4.海帶多糖對(duì)大鼠頜下腺輻射誘導(dǎo)的細(xì)胞凋亡具有抑制作用。 5.海帶多糖對(duì)輻射誘導(dǎo)的大鼠頜下腺細(xì)胞損傷具有保護(hù)作用。 6.海帶多糖對(duì)人鼻咽癌HONE1和CNE2細(xì)胞增殖有抑制作用。 7.海帶多糖對(duì)人鼻咽癌HONE1和CNE2細(xì)胞抑制具有濃度依賴效應(yīng)。 8.海帶多糖對(duì)人鼻咽癌HONE1移植瘤的抑瘤機(jī)制是促進(jìn)癌細(xì)胞的凋亡。
[Abstract]:Objective: radiation therapy is the main treatment for nasopharyngeal carcinoma and other head and neck malignant tumors. The conventional radiation field of radiotherapy in patients with nasopharyngeal carcinoma, such as head and neck cancer, is mainly on both sides. The salivary gland, especially the parotid gland is located in the target area of the radiotherapy. The radiation causes the injury of the salivary gland tissue, the gland dysfunction and the decrease of saliva secretion. Oral xerostomia has a serious impact on the quality of life in patients after radiotherapy. At present, the radiation induced dry mouth disease is still treated with comprehensive symptomatic treatment and lack of effective prevention and treatment. It is important to study the mechanism of radiation induced injury of salivary glands and find drugs that can both antagonize radiation and inhibit tumor. This study is of important clinical significance. Deoxynucleotidyl terminal transferase mediated dTP nick end labeling (TdT-mediated dUTP nick end labeling, TUNEL), electron microscope Pathomorphology, immunohistochemical staining, cell culture, cytotoxicity test (MTT), nude mouse transplanted tumor model, reverse transcription polymerase chain reaction (reverse transcription polymerase chain) R) detection techniques are designed to understand the early (1-3 days) conditions of radiation induced damage to the submandibular gland of rats by different radiation doses. After determining the radiation dose of radiation induced salivary gland injury and exploring the mechanism of injury, the intervention of LJP drugs and the observation of its protective effect on the radiation injury of the submandibular gland and the observation of LJP for human nasopharyngeal carcinoma are observed. HONE1 and CNE2 cell proliferation and the effect of human nasopharyngeal carcinoma (nasopharyngeal carcinoma) nude mice transplanted tumor were affected, and the mechanism of LJP against human nasopharyngeal carcinoma cells was discussed, which provided experimental basis for the anti radiation of LJP salivary gland and anti nasopharyngeal carcinoma.
Methods: This study was divided into three parts: the first part, the effect of different doses of 60Co Y ray on the expression and morphology of the apoptosis related factors of submandibular gland in rats; the second part, the protective effect of Laminaria Polysaccharide on 60Co Y ray induced injury of submandibular gland; the third part, the inhibition of Laminaria Polysaccharide on human nasopharyngeal carcinoma cell lines in nude mice The first part of the experimental method: 48 Wistar rats were divided into two groups: (1) the normal control group (n=12); (2) radiotherapy 7.5Gy group (n=12); (3) radiotherapy 15Gy group (n=12); (4) radiotherapy 22.5Gy group (n=12). The radiotherapy group was irradiated with each one-time dose of 15Gy gamma -ray, while the control group was not irradiated. 1 D, 3 D, 6 rats in each group after radiotherapy. After the submandibular gland was fixed, the rats were frozen and frozen. The immunohistochemical SP method was used to detect the expression of P53 and Caspase-3 and the apoptosis of the cells by TUNEL method. 1 submandibular gland scanning electron microscopy (Transmission electron microscope, SEM) were taken in each group to observe the morphological and pathological changes of the submandibular gland. The second part of the experimental methods: 24 Wistar rats The random grouping principles were divided into: (1) the normal control group (n=6); (2) LJP high dose radiotherapy group (300mg/kg/ only / LJP) (n=6); (3) LJP low dose radiotherapy group (30m/kg/ only / day LJP) (n=6). (4) the radiotherapy control group (n=6). The 3 D before radiotherapy and the latter 3 D were given the above drugs. The control group was not irradiated. 6 rats in each group were taken from the submandibular gland in each group at third days after the radiotherapy. After the fixation, the frozen section was fixed, the expression of P53, Caspase-3 expression and the TUNEL method were used to detect the apoptosis of.15 only Wistar rats by electron microscopy, and divided into 7.5Gy, 15Gy, and 22.5 Gy three doses group (1 normal control). Group (n=1); (2) LJP high dose radiotherapy group (n=1); LJP low dose radiotherapy group (n=1); (n=1); (n=1); (5) sucrose negative control group (n=1), with the above method, in the morning after radiotherapy, the submandibular gland tissue of the rat was examined by electron microscopy, and the morphological and pathological changes of the submandibular gland were observed. The experimental method of the application of MTT: the application of MTT The inhibitory effects of LJP on the proliferation of human NPC cell lines (HONE1 and CNE2).30 were randomly divided into groups: (1) NS (normal control group: NSO. lml/lOg/d) (n=6); (2) LJP 12.5 (LJP12.5mg/kg/d) (n=6); (25); (positive control group: 2). The cell line HONE1 established a nude mouse model of subcutaneous transplantation tumor. The tumor suppressor rate was calculated by grouping drugs in vivo and the tumor suppressor rate was calculated. RT-PCR was used to detect the expression of Bax, Bcl-2, Caspase-3,8,9 messenger ribonucleic acid (mRNA), Bcl-2, Caspase-3,8,9.
Results: the first part: (1) the expression of p53 was as follows: 7.5 Gvld, there was no significant difference between the 3D irradiation group and the control group (P0.05), and there was a significant statistical difference between the 15 Gy1d and the control group (P0.01), and the difference between the 22.5Gy3d irradiation group and the control group was statistically significant (P0.05); the difference between 1D and between 3D and 15 Gy irradiated groups was different. There was significant statistical significance (P0.01). There was no significant difference between 1 D and 3D in 7.5 Gy and 22.5 Gy irradiated groups (P0.05). (2) Caspase-3 expression was 7.5 Gy, 1 D and 3D in 22.5 Gy irradiation group, and 15 Gy group was significantly different from the control group. There was a statistically significant difference between the 15 irradiated group and the control group. The difference between 1D and 3D in P0.05.15 Gy irradiation group was statistically significant (P0.05); 7.5 Gy, 22.5 Gy irradiation group had no significant difference between 1 D and 3D (P0.05). (3) TUNEL staining expression was statistically significant (7.5); 15 The difference was statistically significant (P0.05); the difference between 3D and control group in 15 Gy irradiation group was statistically significant (P0.01); 7.5 G, 15 Gy, 1 D in 22.5 Gy irradiation group had no statistical significance (P0.05), 7.5 G, 15 Gy, and 22.5 differences between groups. Group serous acinar cells and ductal cells, complete nuclear membrane and disappearance of nucleolus. Heterochromatin integrates lumps and sides in the inner part of the nuclear membrane. In the cytoplasm, the rough endoplasmic reticulum dilated slightly, mitochondria swollen slightly, and the crista blurred. Cell membrane crinkle, mitochondria swollen in cytoplasm, crista breaks, crest breaks, nuclei complete, and nuclei are intact. .15Gy radiotherapy group had serous acinar cells and ductal cells, cell shrinkage, increased electron density, complete nuclear membrane, nucleolus disappearing, heterochromatin in nucleus increased obviously, agglutinating lump and edge of the inner membrane; rough endoplasmic reticulum decreased and expanded obviously, and the granules were arranged in disorder, mitochondrial structure model It is not clear that the serous acinus cells and ductal cells in the.22.5Gy radiotherapy group are crinkled, the electron density is increased, the nuclear membrane is incomplete, the heterochromatin is integrated into the inner nucleus of the nuclear membrane and the nuclear perinuclear gap widened, and the rough endoplasmic reticulum in the cytoplasm is greatly reduced, and the structure is disorganized, the secretory granules disappear, the remnants of the remnants are a small amount of mitochondria, and the nucleus is in the nucleus. The heterochromatin began to increase. The second part: (1) the expression of p53 was: the difference between the radiotherapy group and the control group was statistically significant (P0.05); the difference of the group in the radiotherapy group was statistically significant (P0.05), and the number of apoptosis in the high dose LJP group was the lowest. (P0) the expression of Caspase-3 was statistically significant (P0 .05); there was no significant difference between group LJP30 and group LJP300 (P0.05). Group LJP30, group LJP300 and radiotherapy group had statistical significance (P0.05). (P0.05). (P0.05). (P0.05). (3) TUNEL staining results were statistically significant (P0.05) compared with radiotherapy group (P0.05), and there was no significant difference between the LJP30 group and the group. (4) electron microscopy The results of observation: 7.5 Gy, 15 Gy, 22.5 Gy three groups of nuclei, mitochondria, endoplasmic reticulum and secretory vesicles, with the increase of dosage, showed the characteristics of damage aggravation, LJP30. LJP300 group cells were compared with radiotherapy, and the sucrose control group was compared with light cell structure damage and protective effect on cells. Third parts: (1) MTT results: LJP to HONE1 The IC10 of the cells was 76.85 mu g/ml, IC20 was 115.31 mu g/ml, IC30 was 153.77 mu g/ml, IC10 of CNE2 cells was 18.92 mu g/ml, IC20 57.38 micron g/ml. Compared with P0.01), the average inhibitory rate of the 12.5mg/kg LJP group was only 16.4% (compared with the NS group, P0.05), and the inhibitory effect was not obvious, while the average inhibition rate of the 25mg/kg and 50mg/kg LJP groups was 33.7% (compared with the NS group, P0.05) and 47% (P0.01). There were statistical significance (P0.05) in the comparison of group NS, and the expression of Bcl-2 mRNA in group LJP12.5, LJP25, LJP50 and DDP2 was statistically significant (P0.05), LJP 12.5, LJP 25, LJP 50, compared with the control group, there were statistically significant differences. The difference was statistically significant (P0.05), and the expression of Bcl-2mRNA: LJP25/LJP12.5LJP 50DDP2, the difference between the groups was statistically significant (P0.05).LJP 12.5, LJP 25, LJP 50, DDP2 group Caspase-3, Caspase-9 mRNA expression was statistically significant compared with the control group. P0.05.Caspase-3 mRNA expression: DDP2 LJP 50 LJP 25 LJP 12.5, and there was a significant difference in expression between each group (P0.05), Caspase-8 mRNA expression: NS group and LJP12.5 group, there was no difference between 50 and 25. No difference was found, and the expression was lower than that of the DDP2 treatment group.
Conclusion:
1.60Co gamma irradiation can induce early apoptosis of rat submandibular gland.
2.60Co - ray (7.5Gy, 15 Gy, 22.5 Gy) irradiation induced apoptosis of submandibular gland cells in a dose-response relationship.
3.15 the injury of submandibular gland cells induced by Gy irradiation was in the early stage (1-3 days) at the stage of repair and apoptosis.
4. Laminaria japonica polysaccharide inhibited the apoptosis induced by radiation-induced apoptosis in the submandibular gland of rats.
5. Laminaria japonica polysaccharide has protective effect on radiation induced injury of rat submandibular gland cells.
6. Laminaria japonica polysaccharide inhibited the proliferation of HONE1 and CNE2 cells in NPC.
7. Laminaria japonica polysaccharide has a concentration dependent effect on HONE1 and CNE2 cell inhibition in NPC.
8. the inhibitory mechanism of Laminaria japonica polysaccharide on human nasopharyngeal carcinoma HONE1 xenografts is to promote the apoptosis of cancer cells.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2012
【分類號(hào)】：R739.63
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本文編號(hào)：1960240