發(fā)布時間：2018-09-02 10:06

【摘要】：目的及意義 隨著微波技術(shù)在軍事、醫(yī)療、工業(yè)、通信及農(nóng)業(yè)生產(chǎn)等方面的廣泛應(yīng)用，生物體不可避免地受到微波輻射的影響。研究表明，微波輻射對生物體的多個系統(tǒng)具有損傷作用，其對免疫系統(tǒng)的損傷及醫(yī)學(xué)防護是近年來生物電磁學(xué)研究的熱點之一。然而，微波輻射致免疫損傷的機制不明，且目前尚缺乏有效預(yù)防微波輻射致免疫損傷的藥物。本文旨在研究中藥復(fù)方制劑安多霖對微波輻射所致免疫損傷的預(yù)防作用及有效劑量，探討NK細(xì)胞的重要活化性受體NKG2D在其中的作用，并對NKG2D/ERK信號通路在微波輻射致免疫損傷中的作用進行研究，為微波輻射致免疫損傷機制的闡明、有效防護藥物的選擇和應(yīng)用提供理論基礎(chǔ)，具有重要的現(xiàn)實意義。 材料和方法 本課題分為整體動物實驗和離體細(xì)胞實驗兩部分。 一、整體動物實驗選用250只二級雄性Wistar大鼠，分為安多霖2w及4w預(yù)防實驗。各實驗大鼠125只，隨機分為正常對照組、輻射對照組及0.75、1.5、3g/(kg d)藥物組。大鼠連續(xù)給藥2w或4w后，30mW/cm2微波輻射15min，于輻射（停藥）后6h、7d、14d，應(yīng)用血細(xì)胞分析儀檢測外周血白細(xì)胞、淋巴細(xì)胞數(shù)量，放免法檢測血清IL-2和IL-4濃度，流式細(xì)胞儀檢測外周血CD3、CD4、CD8淋巴細(xì)胞亞群（計算CD4+/CD8+比值），光鏡及電鏡觀察胸腺和脾臟組織結(jié)構(gòu)及超微結(jié)構(gòu)改變，Western Blot檢測脾臟組織NKG2D蛋白表達(dá)。 二、離體細(xì)胞實驗1.將培養(yǎng)的NK92細(xì)胞隨機分為假輻射組及10、30、50mW/cm2輻射組，分別應(yīng)用10、30、50mW/cm2微波輻射細(xì)胞5min，于輻射后1h及24h，采用倒置相差顯微鏡觀察細(xì)胞形態(tài)，流式細(xì)胞儀檢測細(xì)胞凋亡、壞死和細(xì)胞周期，乳酸脫氫酶法檢測NK92細(xì)胞對K562靶細(xì)胞的殺傷活性，建立微波輻射致NK92細(xì)胞損傷模型；2.采用30mW/cm2微波輻射NK92細(xì)胞5min，輻射后1h、6h及12h，應(yīng)用Real-time PCR、Western Blot和圖像分析技術(shù)檢測細(xì)胞中NKG2D、perforin蛋白和mRNA以及ERK1/2、p-ERK1/2表達(dá)的改變；3.于輻射前30min加入50μmol/l U0126進行干預(yù)，Western Blot檢測U0126干預(yù)及微波輻射后1h，ERK1/2、p-ERK1/2及perforin表達(dá)。 實驗結(jié)果 一、大鼠外周血免疫功能指標(biāo)變化：2w預(yù)防實驗30mW/cm2微波輻射后14d，外周血白細(xì)胞數(shù)及CD4~+/CD8~+比值較正常對照組明顯下降（p0.05或p0.01）；與輻射對照組相比，1.5、3g/(kg d)藥物組在輻射后14d，淋巴細(xì)胞、白細(xì)胞數(shù)和CD4~+/CD8~+比值明顯升高（p0.05或p0.01）。0.75g/(kg d)藥物組外周血白細(xì)胞、淋巴細(xì)胞計數(shù)與輻射對照組相比無明顯差異。IL-2和IL-4血清濃度各組間相比無明顯差異。4w預(yù)防實驗結(jié)果與2w預(yù)防實驗結(jié)果相似。 二、大鼠胸腺及脾臟組織學(xué)和超微結(jié)構(gòu)改變：2w預(yù)防實驗30mW/cm2微波輻射后6h，胸腺組織結(jié)構(gòu)變化輕微，輻射后7d病變恢復(fù)；脾臟于微波輻射后6h和7d，白髓淋巴細(xì)胞核染色質(zhì)濃縮、固縮、邊移，紅髓和白髓分界不清，紅髓血竇充血；輻射后14d，病變基本恢復(fù)。輻射后7d超微結(jié)構(gòu)觀察見脾臟凋亡、壞死的淋巴細(xì)胞增多。0.75g/(kg d)藥物組胸腺及脾臟組織學(xué)結(jié)構(gòu)與輻射對照組相似，1.5、3g/(kg d)藥物組組織學(xué)及超微結(jié)構(gòu)損傷明顯減輕。4w預(yù)防實驗大鼠胸腺和脾臟組織學(xué)及超微結(jié)構(gòu)變化規(guī)律與2w預(yù)防實驗結(jié)果相似。 三、大鼠脾臟組織NKG2D表達(dá)變化：30mW/cm~2微波輻射后6h，脾臟組織NKG2D表達(dá)較正常對照組明顯降低（p0.01），1.5、3g/(kg d)藥物組NKG2D表達(dá)較輻射對照組明顯升高（p0.05或p0.01），0.75g/(kg d)藥物組與輻射對照組相比無明顯差異。 四、NK92細(xì)胞形態(tài)、凋亡與壞死率、細(xì)胞周期改變：與假輻射組相比，輻射后1h，10、30、50mW/cm2組細(xì)胞輪廓不規(guī)則，折光性降低，G0/G1期細(xì)胞百分比明顯增加（p0.01）， S期細(xì)胞百分比明顯降低（p0.05或p0.01），細(xì)胞壞死率升高（p0.05或p0.01）；30、50mW/cm~2組G2/M期細(xì)胞百分比亦明顯增加（p0.05或p0.01），細(xì)胞凋亡率升高（p0.05或p0.01）。輻射后24h，30、50mW/cm~2組細(xì)胞凋亡率較假輻射組升高（p0.05）。輻射后1h及24h，10mW/cm2組細(xì)胞凋亡率與假輻射組相比無明顯差異。 五、NK92細(xì)胞殺傷活性變化：輻射后1h，30、50mW/cm2組NK92細(xì)胞對K562細(xì)胞的殺傷活性較假輻射組明顯降低（p0.01），10mW/cm~2組與假輻射組相比無明顯差異。 六、NK92細(xì)胞NKG2D蛋白及基因表達(dá)變化：30mW/cm~2微波輻射后6h，NK92細(xì)胞NKG2DmRNA及蛋白表達(dá)明顯下降（p0.05或p0.01），輻射后12h與假輻射組相比無明顯差異。 七、NK92細(xì)胞NKG2D活化的效應(yīng)分子perforin蛋白及基因表達(dá)變化：30mW/cm2微波輻射后1h，NK92細(xì)胞perforin mRNA表達(dá)明顯下降（p0.05），輻射后1h及6h蛋白表達(dá)明顯下降（p0.05或p0.01），輻射后12h與假輻射組相比無明顯差異。 八、NK92細(xì)胞p-ERK1/2表達(dá)變化：30mW/cm~2微波輻射后1h，NK92細(xì)胞p-ERK1/2表達(dá)明顯低于假輻射組（p0.01），輻射后6h、12h，p-ERK1/2表達(dá)與假輻射組相比無明顯差異。 九、U0126干預(yù)后p-ERK1/2及perforin表達(dá)變化：U0126干預(yù)及30mW/cm~2微波輻射后，NK92細(xì)胞p-ERK1/2和perforin表達(dá)較單純輻射組明顯降低（p0.05或p0.01）。 結(jié)論 一、預(yù)防性給予1.5、3g/(kg d)安多霖2w或4w對30mW/cm~2微波輻射引起的免疫功能和免疫器官結(jié)構(gòu)損傷有保護作用，預(yù)防性給予0.75g/(kg d)安多霖2w或4w保護作用不明顯。 二、連續(xù)給藥2w或4w預(yù)防效果無明顯差別；安多霖對微波輻射致免疫損傷的最佳有效預(yù)防劑量為1.5g/(kg d)；2w為最佳給藥周期。 三、30，，50mW/cm~2微波輻射可損傷NK92細(xì)胞，表現(xiàn)為細(xì)胞形態(tài)不規(guī)則、細(xì)胞凋亡及壞死率升高、增殖活性及殺傷活性降低，10mW/cm2微波輻射對NK92細(xì)胞凋亡及殺傷活性無明顯影響。 四、30mW/cm~2微波輻射可致NKG2D及perforin蛋白及基因表達(dá)下降。 五、微波輻射后ERK信號通路活化對NK92細(xì)胞perforin表達(dá)有正向調(diào)控作用，微波輻射使NKG2D/ERK/perforin通路活化受到抑制。 六、安多霖預(yù)防微波輻射致免疫損傷的作用可能通過促進NKG2D表達(dá)，活化NKG2D/ERK/perforin信號通路來實現(xiàn)。
[Abstract]:Purpose and significance
With the wide application of microwave technology in military, medical, industrial, communication and agricultural production, organisms are inevitably affected by microwave radiation. Studies have shown that microwave radiation can damage many systems of organisms, and its damage to the immune system and medical protection is one of the hotspots of bioelectromagnetism in recent years. 1. However, the mechanism of microwave-induced immune damage is unknown, and there is no effective drug to prevent microwave-induced immune damage at present. The purpose of this paper is to study the preventive effect and effective dosage of andolin on microwave-induced immune damage, and to explore the role of NKG2D, an important activator receptor of NK cells, in this process, and its effect on N. The role of KG2D/ERK signaling pathway in microwave-induced immune injury is studied, which provides theoretical basis for elucidating the mechanism of microwave-induced immune injury and for the selection and application of effective protective drugs.
Materials and methods
The research is divided into two parts: the whole animal experiment and the in vitro cell experiment.
Firstly, 250 male Wistar rats were divided into two weeks and four weeks prophylaxis test. 125 rats were randomly divided into normal control group, radiation control group and 0.75, 1.5, 3 g / (kg d) drug group. After 2 or 4 weeks of continuous administration, 30 mW / cm 2 microwave irradiation for 15 minutes, 6 h, 7 d, 14 d after radiation (withdrawal), blood cell analyzer was used. The number of white blood cells and lymphocytes in peripheral blood were detected. The serum levels of IL-2 and IL-4 were detected by radioimmunoassay. The peripheral blood CD3, CD4 and CD8 lymphocyte subsets (calculated CD4 +/CD8 +) were detected by flow cytometry. The histological and ultrastructural changes of thymus and spleen were observed by light and electron microscopy. The expression of NKG2D protein in spleen was detected by Western Blot.
2. In vitro cell experiment 1. NK92 cells were randomly divided into sham radiation group and 10,30,50 mW/cm 2 radiation group. NK92 cells were irradiated with 10,30,50 mW/cm 2 microwave for 5 minutes. The morphology of NK92 cells was observed by inverted phase contrast microscope at 1 h and 24 h after irradiation. Cell apoptosis, necrosis and cell cycle were detected by flow cytometry. NK92 cells were detected by lactate dehydrogenase method. NK92 cells were injured by microwave irradiation for 5 min, 1 h, 6 h and 12 h after irradiation. Real-time PCR, Western Blot and image analysis were used to detect the expression of NKG2D, perforin protein and mRNA, as well as ERK1/2, p-ERK1/2. The expression of ERK1/2, p-ERK1/2 and perforin was detected by Western Blot 1 hour after U0126 intervention and microwave irradiation.
experimental result
1. Changes of immune function in peripheral blood of rats: The number of white blood cells and the ratio of CD4~+/CD8~+ in peripheral blood were significantly decreased 14 days after 30 mW/cm2 microwave irradiation (p0.05 or p0.01), and the number of lymphocytes, white blood cells and the ratio of CD4~+/CD8~+ were significantly increased 14 days after irradiation (p0.05 or p0.01). There was no significant difference in peripheral blood leukocyte and lymphocyte counts between the two groups. There was no significant difference in serum IL-2 and IL-4 concentrations between the two groups.
2. Histological and ultrastructural changes of thymus and spleen in rats: 2 weeks after 30 mW/cm2 microwave irradiation, the histological changes of thymus were slight, and the pathological changes of thymus were restored 7 days after irradiation; 6 hours and 7 days after microwave irradiation, the chromatin of lymphocyte nucleus of white pulp was condensed, condensed, margined, the demarcation between red pulp and white pulp was unclear, and the blood sinus of red pulp was congested 14 days after irradiation. The histological structure of thymus and spleen in the drug group was similar to that in the radiation control group. The histological and ultrastructural damage of thymus and spleen in the 1.5 and 3 g / (kg d) drug group was significantly alleviated. The rule is similar to that of 2W preventive test.
Third, the expression of NKG2D in spleen tissue of rats: 6 hours after 30 mW/cm~2 microwave irradiation, the expression of NKG2D in spleen tissue was significantly lower than that of normal control group (p0.01), and the expression of NKG2D in 1.5, 3 g/(kg d) drug group was significantly higher than that of radiation control group (p0.05 or p0.01). There was no significant difference between 0.75 g/(kg d) drug group and radiation control group.
Fourthly, NK92 cell morphology, apoptosis and necrosis rate, cell cycle changes: compared with sham radiation group, 1 h, 10, 30, 50 mW / cm 2 group cells outline irregular, refractive decreased, G0 / G1 phase cell percentage significantly increased (p0.01), S phase cell percentage significantly decreased (p0.05 or p0.01), cell necrosis rate increased (p0.05 or p0.01); The percentage of apoptotic cells in phase I was also significantly increased (p0.05 or p0.01), and the apoptotic rate was increased (p0.05 or p0.01). The apoptotic rate in 30,50 mW/cm~2 group was higher than that in sham radiation group at 24 h, 30,50 mW/cm~2 group (p0.05).
Fifth, NK92 cell killing activity changes: 1 hour after radiation, 30,50 mW/cm 2 group NK92 cell killing activity to K562 cells was significantly lower than the sham radiation group (p0.01), 10 mW/cm~2 group and sham radiation group compared with no significant difference.
6. Changes of NKG2D protein and gene expression in NK92 cells: At 6 hours after 30 mW/cm~2 microwave irradiation, NKG2D mRNA and protein expression in NK92 cells decreased significantly (p0.05 or p0.01). There was no significant difference between the two groups at 12 hours after irradiation.
Seventh, the expression of NKG2D-activated effector molecule perforin protein and gene in NK92 cells: 1 hour after 30 mW/cm 2 microwave irradiation, the expression of perforin mRNA in NK92 cells decreased significantly (p0.05), 1 hour and 6 hours after irradiation (p0.05 or p0.01).
Eighth, the expression of p-ERK1/2 in NK92 cells: 1 hour after 30 mW/cm~2 microwave irradiation, the expression of p-ERK1/2 in NK92 cells was significantly lower than that in sham irradiation group (p0.01). The expression of p-ERK1/2 was not significantly different from that in sham irradiation group at 6 and 12 hours after irradiation.
Ninth, the expression of p-ERK1/2 and perforin after U0126 intervention: After U0126 intervention and 30 mW/cm~2 microwave irradiation, the expression of p-ERK1/2 and perforin in NK92 cells was significantly lower than that in the radiation group (p0.05 or p0.01).
conclusion
First, prophylactic administration of 1.5, 3 g / (kg d) andolin for 2 or 4 weeks has protective effects on immune function and structural damage of immune organs induced by 30 mW/cm~2 microwave irradiation, but prophylactic administration of 0.75 g / (kg d) andolin for 2 or 4 weeks has no obvious protective effects.
Secondly, there was no significant difference in the preventive effect between two weeks or four weeks of continuous administration; the best effective preventive dose of andolin for microwave-induced immune damage was 1.5 g / (kg d); and the best period of administration was two weeks.
Third, 30,50 mW/cm~2 microwave irradiation could damage NK92 cells, which showed irregular cell morphology, increased apoptosis and necrosis rate, decreased proliferation and killing activity. 10 mW/cm~2 microwave irradiation had no significant effect on apoptosis and killing activity of NK92 cells.
Four, 30mW/cm~2 microwave radiation can cause the decrease of NKG2D and perforin protein and gene expression.
Fifthly, the activation of ERK signaling pathway after microwave irradiation can positively regulate the expression of perforin in NK92 cells, and the activation of NKG2D/ERK/perforin pathway is inhibited by microwave irradiation.
Sixthly, the preventive effect of andolin on microwave-induced immune injury may be achieved by promoting NKG2D expression and activating NKG2D/ERK/perforin signaling pathway.
【學(xué)位授予單位】：中國人民解放軍軍事醫(yī)學(xué)科學(xué)院
【學(xué)位級別】：博士
【學(xué)位授予年份】：2012
【分類號】：R363

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