【作者】 罗亚萍；

【导师】 李春香；

【作者基本信息】 河北医科大学 ， 中西医结合基础， 2014， 博士

【摘要】 目的：以900MHz手机频率电磁辐射为干预因素，以大鼠肝脏组织为研究对象，以肝功能、组织形态学、抗氧化酶活性、Nrf2蛋白表达、DNA损伤及损伤修复蛋白ATM、γ-H2AX表达和大鼠肝细胞周期及凋亡的变化为主要观测指标，选择西洋参胶囊和水飞蓟宾胶囊作为实验用药，观察常见手机频率的电磁辐射对大鼠肝损伤的可能机制和西洋参胶囊对其作用。手机频率电磁辐射对大鼠肝脏的影响（论文第一、二、三部分）方法：1造模及分组清洁级SD雄性大鼠50只，体重200~220g。随机分正常组和辐射6d、12d、20d、30d组，共计5个实验组，每组10只，共50只。除正常组不辐射外，其余各组均置辐射笼内，打开自动开关每天4小时，分别连续辐射6d、12d、20d和30d，每天除辐射外正常饲养。2取材及检测指标各组实验结束后禁食12小时，10%水合氯醛腹腔麻醉后处死，股动脉取血离心取血清测ALT、AST含量；取肝脏称重后将相同部位肝组织（约0.3×0.5×0.5cm3）置于4%多聚甲醛溶液固定，用于HE染色；比色法检测肝组织MDA、SOD、GSH、GSH-PX含量；采取免疫组化及Western blot法检测Nrf2及ATM、γH2AX蛋白表达；流式细胞仪检测各组大鼠肝细胞周期和凋亡率。结果：1手机频率电磁辐射对大鼠肝脏功能的影响1各组大鼠一般情况观察各组大鼠的精神状态、进食水量、排泄、皮毛、活动等情况无显著差异。1.2各组大鼠血清ALT、AST的比较与正常组大鼠相比较，辐射30d大鼠血清AST水平显著性增高，（P＜0.05），辐射6d、12d、20d组大鼠无显著变化（P＞0.05）;与正常组大鼠相比较，辐射6d、12d、20d、30d组大鼠血清ALT水平无显著变化（P＞0.05）。1.3各组大鼠肝脏组织形态学变化的比较正常组肝组织肝小叶的结构清晰完整，肝细胞界限明显，大小基本相同，1~2个圆形或类圆形细胞核位于细胞中间。辐射6d组肝小叶结构紊乱，可见细胞界限不清，区域性肝细胞变性，细胞核消失，细胞浆出现空泡样变化，组织形态学异常。12d组肝小叶结构完整，肝细胞分界清，个别细胞核固缩或消失，组织形态学异常。20d组肝小叶结构完整，肝细胞分界清，个别细胞核固缩或消失。30d组肝小叶结构完整，肝细胞分界清，出现较明显的肝细胞核固缩现象，组织形态学异常。2手机频率电磁辐射对大鼠肝氧化损伤及抗氧化酶、Nrf2蛋白表达的影响2.1各组大鼠肝组织MDA、SOD、GSH、GSH-PX含量的比较与正常组大鼠相比，各辐射组大鼠肝组织MDA水平均显著增高（P＜0.05）。辐射12d、30d组大鼠肝组织SOD含量均显著减少（P＜0.05）；辐射6d、20d组大鼠SOD含量无显著性变化（P＞0.05）。各辐射组大鼠肝组织GSH水平均显著减少（P＜0.05）。辐射20d、30d组大鼠肝组织GSH-PX水平均显著降低（P＜0.05）。2.2免疫组化法检测大鼠肝细胞Nrf2蛋白表达正常组大鼠肝细胞浆中有Nrf2表达，肝细胞核内无明显表达，各辐射组均细胞核有Nrf2表达。与正常组相比，辐射6d、12d、20d、30d，Nrf2在肝细胞的表达出现先增强，后稍弱再增强的变化，Nrf2蛋白表达由强到弱顺序为：辐射6d＞12d＞30d＞20d＞正常组。辐射6d与12d之间差异不显著；20d与30d之间差异不显著。但辐射6d、12d与20d、30d之间差异显著（P＜0.05）。2.3Western blot检测各组大鼠肝组织Nrf2蛋白表达与正常组相比，各辐射组大鼠肝组织Nrf2蛋白表达平均灰度比值明显增强（P＜0.01）；与免疫组化结果相符，辐射6d、12d、20d、30d，Nrf2在肝细胞的表达出现先增强，后稍弱再增强的变化，Nrf2蛋白表达由强到弱顺序为：辐射6d＞12d＞30d＞20d＞正常组。3手机频率电磁辐射对大鼠肝细胞DNA损伤修复蛋白ATM、H2AX表达及细胞周期和凋亡率的影响3.1免疫组织化学法检测ATM、γH2AX蛋白在各组大鼠肝组织的表达ATM蛋白在各组大鼠肝细胞核和细胞浆均有表达。与正常组大鼠相比，辐射12d、20d、30d组大鼠肝细胞核和细胞浆中表达均显著增强（P＜0.01），随着辐射时间的延长，ATM蛋白表达平均光密度增加（P＜0.05）。γH2AX在各组大鼠肝细胞核和细胞浆均有表达，与正常组大鼠相比，辐射6d、12d、20d、30d组大鼠肝细胞核和细胞浆中表达均显著增强（P＜0.05；P＜0.05；P＜0.05；P＜0.01）；随着辐射时间的延长，γH2AX蛋白表达增加。3.2Western blot检测ATM、H2AX蛋白在大鼠肝组织的表达与正常组大鼠比较，辐射6d、12d、20d、30d组大鼠肝组织ATM蛋白的平均灰度比值逐渐增加（P＜0.01）。与正常组大鼠比较，辐射6d、12d、20d、30d组大鼠肝组织H2AX蛋白的平均灰度比值显著增加，有统计学意义，（P＜0.05，P＜0.01，P＜0.01，P＜0.01）。3.3各组大鼠肝细胞周期的比较G0/G1期细胞：与正常组相比，辐射6d、12d、20d、30d组大鼠G0/G1期细胞比例均显著增加（P＜0.01；P＜0.05；P＜0.01；P＜0.01）。S期%细胞：与正常组相比，辐射6d、12d、20d组大鼠S期%细胞无显著性变化（P＞0.05）；辐射30d大鼠S期%细胞数量显著减少（P＜0.05）。G2/M期%细胞：与正常组相比，辐射6d、12d、20d组大鼠G2/M期%细胞均显著性减少（P＜0.01）。3.4各组大鼠肝细胞凋亡率的比较与正常组相比，辐射6d、12d、20d、30d组大鼠肝细胞凋亡率极显著增加（P＜0.01）；与辐射6d、12d和20d组相比，辐射30d组增加有显著性差异（P＜0.05）。结论：1长时间手机频率的电磁辐射是一种致病因素，可导致肝组织形态学损伤，具有时间效应关系。2手机频率电磁辐射致大鼠肝损伤与抗氧化酶活性的变化及Nrf2表达变化具有相关性。3手机频率电磁辐射致大鼠肝组织形态学异常与肝细胞DNA损伤，激活修复相关的ATM和H2AX蛋白表达，影响细胞周期和细胞凋亡。西洋参胶囊对手机频率电磁辐射大鼠肝损伤的干预作用（论文第四部分）方法：1分组清洁级SD雄性大鼠40只，分为正常组、模型组（辐射12d组）、水飞蓟宾组（辐射12d加水飞蓟宾组）、西洋参胶囊组（辐射12d加西洋参胶囊组），各10只。2取材及检测指标各组实验结束后禁食12h，10%水合氯醛腹腔麻醉后处死，股动脉取血离心取血清测ALT、AST含量；取肝脏称重后将相同部位肝组织（约0.3×0.5×0.5cm3）置于4%多聚甲醛溶液固定，用于HE染色；比色法检测肝组织MDA、SOD、GSH、GSH-PX含量；采取免疫组化及/或Western blot法检测Nrf2及ATM、γH2AX蛋白表达；采用流式细胞法检测各组大鼠肝细胞周期和凋亡率。结果：1西洋参胶囊对辐射12d大鼠模型肝脏组织形态学的干预作用正常组大鼠肝组织细胞结构完整，分界清晰，细胞的大小比较一致，核位于细胞中间，胞质丰富。模型组大鼠肝小叶结构完整，肝细胞核缩小或部分消失，核固缩明显。与模型组相比，水飞蓟宾组和西洋参胶囊组大鼠肝细胞萎缩明显减轻，接近正常。2西洋参胶囊对辐射12d大鼠模型肝脏组织氧化损伤指标的干预作用与正常组比较，模型组MDA含量显著升高（P＜0.05），SOD、GSH含量显著降低（P＜0.05）。与模型组比较，水飞蓟宾组MDA含量显著降低（P＜0.05），SOD、GSH、GSH-PX含量显著升高（P＜0.05）；西洋参胶囊组MDA含量显著降低（P＜0.05），SOD、GSH含量显著升高（P＜0.01，P＜0.05）。3西洋参胶囊对辐射12d大鼠模型肝脏组织Nrf2蛋白表达的干预作用3.1免疫组化检测结果正常组仅在大鼠肝细胞浆中有Nrf2蛋白表达，肝细胞核内无明显表达，其余三组均主要在细胞核有Nrf2蛋白表达。与正常组比较，模型组大鼠肝脏组织Nrf2蛋白表达平均吸光度值显著升高（P＜0.05），胞浆和胞核中均有表达。与模型组比较，水飞蓟宾组和西洋参胶囊组大鼠肝脏组织Nrf2蛋白表达平均吸光度值均显著降低（P＜0.05）。3.2Western blot检测结果与正常组比较，模型组大鼠肝脏组织Nrf2蛋白表达平均灰度比值升高（P＜0.01）。与模型组比较，水飞蓟宾组和西洋参胶囊组大鼠肝脏组织Nrf2蛋白表达平均灰度比值均降低（P＜0.05，P＜0.01）。4西洋参胶囊对辐射12d大鼠模型肝脏组织ATM、H2AX的干预作用与正常组比较，辐射后大鼠肝组织ATM平均灰度比值显著增加，表达增强（P＜0.05）。与模型组比较，水飞蓟宾组大鼠肝组织ATM平均灰度比值显著降低，表达减弱（P＜0.05）；西洋参胶囊组大鼠组织ATM平均灰度比值显著降低，表达减弱（P＜0.01）。与正常组比较，辐射后大鼠肝组织H2AX平均灰度比值显著增加，表达增强（P＜0.01）。与模型组比较，水飞蓟宾组大鼠肝组织H2AX平均灰度比值显著降低，表达减弱（P＜0.05）；西洋参胶囊组大鼠组织H2AX平均灰度比值显著降低，表达减弱（P＜0.01）。5西洋参胶囊对辐射12d大鼠模型肝细胞周期和细胞凋亡率的干预作用5.1西洋参胶囊对辐射12d大鼠模型肝细胞周期的干预作用与正常组大鼠相比较，辐射后大鼠肝细胞G0/G1期%显著增加（P＜0.01）。与模型组比较，水飞蓟宾组大鼠G0/G1期肝细胞比例无显著变化（P＞0.05）；西洋参胶囊组大鼠G0/G1期%肝细胞数极显著降低（P＜0.01），接近正常。与正常组大鼠相比较，辐射后大鼠肝细胞S期%无显著性变化（P＞0.05）。与模型组比较，水飞蓟宾组大鼠肝细胞S期%明显降低（P＜0.01）；而西洋参胶囊组大鼠肝细胞S期%无显著变化（P＞0.05）。与正常组大鼠相比较，辐射后大鼠肝细胞G2/M期%极显著减少（P＜0.01）。与模型组比较，水飞蓟宾组大鼠肝细胞G2/M期%无显著性差异（P＞0.05）；西洋参胶囊组大鼠肝细胞G2/M期%极显著增高（P＜0.01）。5.2西洋参胶囊对辐射12d大鼠模型肝细胞凋亡率的干预作用与正常组大鼠相比较，辐射后大鼠肝细胞凋亡率显著增加（P＜0.01）。与辐射组比较，水飞蓟宾组大鼠无显著差异（P＞0.05）；西洋参胶囊组大鼠肝细胞凋亡率显著性降低（P＜0.01）。结论：1长时间手机频率电磁辐射是一种致病因素，可导致肝组织损伤。其致病特点归属六淫之温热之邪，可使气阴耗伤。西洋参具有益气养阴作用，主治气阴不足之证。西洋参胶囊对辐射12d大鼠模型肝损伤具有干预作用。2西洋参胶囊可改善肝组织形态学异常变化，与降低氧化损伤、降低Nrf2在肝细胞的表达、降低ATM和H2AX蛋白表达，影响细胞周期和细胞凋亡有关。3西洋参胶囊对手机频率电磁辐射所致肝损伤模型具有保护作用。更多还原

【Abstract】 Objective: This study investigated the possible mechanism of the injuryeffects of cellular phone electromagnetic radiation on mice liver tissues andthe intervention effects of American Ginseng and silymarin capsules on theinjury by observing the changes of liver function, histomorphology,antioxidase activity, Nrf2protein expression, DNA injury, expression of theinjury repair proteins ATM and γ-H2AX, and the mice liver proliferation cycleand apoptosis.Effects of cellular phone electromagnetic radiation on mice liver tissuesMethods:1Animal models and groups: Fifty clean grade SD male mice with thebody weight of200-220g were randomized into one normal group and fourirradiation groups with10mice in each group. The four irradiation groupswere divided into four groups with each group receiving irradiation for6,12,20and30days in the irradiation cage. The normal group did not receive anyirradiation. All the mice received normal feeding.2Sampling and testing parameters: After the experiment in each group,the mice were fasted for12hours, the mice were sacrificed by injecting10%chloralhydrate into the peritoneum of the mice. Blood sample was taken fromthe femoral artery and centrifuged. The blood serum was used to test the ALTand AST contents. The liver was taken and weighed, and some liver tissues inthe same location were taken (about0.3×0.5×0.5cm3) and fixed in4%paraformaldehyde solution for HE staining. The contents of MDA, SOD, GSHand GSH-PX in the hepatic tissues were tested by use of chromometry. Theprotein expression of Nrf2, ATM and γH2AX was tested by use ofimmunohistochemistry and Western blot. The cell cycle and apoptosis rate ofthe mice liver were tested by use of flow cytometry. Results：1Effects of cellular phone electromagnetic radiation on mice liver function1.1General observation on the mice in each groupThe mice spirit status, food and water intake, excretion, skin, hair,activities and so on were observed, with no significant differences.1.2Comparison of serum ALT and AST of the mice in every groupCompared with the mice in the normal group, the mice serum AST wassignificantly increased (P<0.05) in the radiation group receiving radiation for30days but did not have significant differences (P>0.05) in the radiationgroups for6,12and20days. Compared with the mice in the normal group, nosignificant (P>0.05) differences existed in the serum ALT in any of theradiation groups for6,12,20or30days.1.3Comparison of the mice liver histomorphologyIn the normal group, the liver tissue had clear and complete structure ofthe liver lobules with clear liver cell boundaries, similar size and one to twocircular or oval cellular nucleus in the center of the cell. In the6-dayirradiation group, the hepatic lobule did not have a clear structure, and thecellular boundary was not clear. Local cellular degeneration was present in theliver, the cellular nucleus disappeared, and the cytoplasm had vacuolardegeneration, indicating abnormal histomorphology. In the12-day and20-dayirradiation groups, the hepatic lobules were complete, the hepatic cells hadclear boundary, and some individual nucleus had pyknosis or disappeared,indicating abnormal histomorphology. In the30-day irradiation group,apparent pyknosis was present in the liver. However, the hepatic lobules werecomplete, and the hepatic cells had clear boundary, indicating abnormalhistomorphology.2Effects of cell phone electromagnetic irradiation on the liver oxidativedamage and the expression of antioxidase and Nrf2protein2.1Comparison of the liver MDA, SOD, GSH and GSH-PX in every groupCompared with the normal group, the MDA level increased significantly(P<0.05) in the mice in every irradiation group, the SOD content decreased significantly (P <0.05) in the12and30day irradiation groups but not in the6or20day irradiation group (P>0.05). The GSH level decreased significantly(P <0.05) in the mice in all the irradiation groups, and the GSH-PX level alsodecreased significantly (P<0.05) in the20and30day irradiation groups ascompared with the normal group.2.2Nrf2protein expression of the mice hepatic cells byimmunohistochemistryNrf2was expressed only in the cytoplasm rather than the nucleus in themice hepatic cells in the normal group, whereas Nrf2was expressed in thenucleus in every irradiation group. Compared with the normal group, the Nrf2expression was first increased, a little decreased and enhanced once again afterirradiation for6,12,20and30days. The order of enhanced expression ofNrf2from strong to weak was6-d>12-d>30-d>20-d>the normal group. Nosignificant difference (P<0.05) existed between6-d and12d groups orbetween20-d and30-d groups. But a significant difference (P<0.05) existed ineither6or12day group as compared with either20or30day group.2.3Nrf2protein expression in the hepatic cells by Western blotCompared with the normal group, the grey level ratio of the Nrf2proteinexpression in the hepatic cells in every irradiation group was significantlyenhanced (P <0.01), consistent with the immunohistochemistry results. Afterirradiation for6,12,20and30days, the Nrf2expression in the hepatic cellswas firstly enhanced, then a little decreased and increased once more, and theorder of Nrf2expression was from strong to weak in the groups:6-d>12-d>30-d>20-d irradiation groups>the normal group.3Effects of cell phone electromagnetic irradiation on the mice hepatic injuryrepair protein ATM and H2AX expression and the cell cycle3.1Expression of ATM and γH2AX proteins in the hepatic tissues in everygroup by immunohistochemistryThe ATM protein was expressed in both the nucleus and cytoplasm in thehepatic cells in every group of mice. Compared with the normal group, theexpression of ATM was enhanced significantly (P<0.01) in the12,20and30 day irradiation groups. With the elongation of the irradiation, the mean opticaldensity of the ATM protein expression increased (P<0.05).γH2AX was also expressed in both the nucleus and cytoplasm in the micehepatic cells. Compared with the normal group, the γH2AX expression wassignificantly enhanced in the6,12,20and30day irradiation groups (P＜0.05,P＜0.05, P＜0.05, P＜0.01, respectively);With the elongation of irradiation,the γH2AX protein expression increased significantly.3.2ATM and γH2AX protein expression in mice hepatic tissues by WesternblotCompared with the normal group, the mean grey level ratio of the ATMprotein in the mice hepatic tissues was gradually increased significantly (P<0.01) after irradiation for6,12,20and30days.Compared with the normal group, the mean grey level ratio of the H2AXprotein in the mice hepatic tissues was gradually increased significantly (P＜0.05，P＜0.01，P＜0.01，P＜0.01) after irradiation for6,12,20and30days,respectively.3.3Comparison of the cell cycleG0/G1stage cells (%): Compared with the normal group, the percentageof the G0/G1stage cells was highly significantly in the6,20and30daygroup(P<0.01;P<0.05; P<0.01; P<0.01).S stage cells (%): Compared with the normal group, the percentage of theS stage cells had no significant (P>0.05) decrease in the6,12and20dayirradiation groups but significant decrease (P<0.01) in the30day irradiationgroup.G2/M stage cells (%): Compared with the normal group, the percentageof the G2/M stage cells had significant decrease (P<0.01) in the6,12and20day irradiation groups. No significant differences (P>0.05) existed among theirradiation groups.3.4Comparison of the Hepatic cell apoptosis rateCompared with the normal group, the hepatic apoptosis rate wassignificantly increased in the6,12,20and30day irradiation groups (P<0.01). Compared with the6,12,and20day irradiation groups,the30-d group hadsignificant differences(P<0.05).Conclusion：1Long-term cell phone electromagnetic irradiation is a cause of diseaseand may lead to the damage to the hepatic histomorphology in a time-efficientmanner.2The cell phone electromagnetic irradiation is closely related to thehepatic damage, the antioxidase activity change or the Nrf2expressionchange.3The abnormal histomorphology caused by cell phone electromagneticirradiation is closely related to the hepatic DNA damage, activation of therepair-related ATM and H2AX protein expression, and changes of the cellcycle and apoptosis.The intervention effects of American ginseng on the hepatic damagecaused by cell phone electromagnetic irradiationMethods：1Grouping: Forty clean grade SD male mice were randomized into thenormal,12-d irradiation group,12-d irradiation plus silymarin group, and12-dirradiation plus American ginseng group, with10mice in each group.2Sampling and testing parameters: After the experiment in each group,the mice were fasted for12hours, the mice were sacrificed by injecting10%chloralhydrate into the peritoneum of the mice. Blood sample was taken fromthe femoral artery and centrifuged. The blood serum was used to test the ALTand AST contents. The liver was taken and weighed, and some liver tissues inthe same location were taken (about0.3×0.5×0.5cm3) and fixed in4%paraformaldehyde solution for HE staining. The contents of MDA, SOD, GSHand GSH-PX in the hepatic tissues were tested by use of chromometry. Theprotein expression of Nrf2, ATM and γH2AX was tested by use ofimmunohistochemistry and Western blot. The cell cycle and apoptosis rate ofthe mice liver were tested by use of flow cytometry. Results：1The intervention effects of American ginseng capsules on the liver histologyof the mice model in the12-d irradiation groupIn the normal group, the cell structure was clear in the mice liver withdefinite demarcation. The cell had consistent size with the nucleus in the cellcenter and rich cytoplasm. In the12-d irradiation group, the hepatic lobuleshad complete structure, the nucleus of the hepatic cells shrank or partiallydisappeared with apparent karyopyknosis. Compared with the modelgroups,the hepatic atrophy was apparently less severe and was nearly normalin the silymarin or the American ginseng group.2The intervention effects of the American ginseng capsules on the oxidativedamage to the hepatic tissues in the12-d groupCompared with the normal group, the hepatic MDA was significantlyincreased (P<0.05) but the hepatic SOD and GSH were significantly decreased(P<0.05) in the12-d group. Compared with the12-d group, the hepatic MDAwas significantly decreased (P<0.05) but the SOD, GSH and GSH-PXcontents were significantly increased (P <0.05) in the12-d irradiation plussilymarin group. Compared with the12-d group, the hepatic MDA wassignificantly decreased (P<0.05) but the SOD and GSH contents weresignificantly increased (P<0.01and P<0.05, respectively) in the12-dirradiation plus American ginseng group.3Intervention effects of American ginseng on the hepatic Nrf2proteinexpression of the12-d irradiation mice group3.1ImmunohistochemistryIn the normal group, the Nrf2protein expression was only in the hepaticcytoplasm of the mice with no apparent expression in the hepatic nucleus. TheNrf2protein expression was mainly in the nucleus in the other three groups.Compared with the normal group, the mean optical density absorbance of thehepatic Nrf2protein expression in the12-d irradiation mice model wassignificantly increased (P<0.01), with expression in both the cytoplasm andthe nucleus. Compared with the12-d irradiation group, the mean optical density absorbance of the hepatic Nrf2protein expression was significantly(P<0.005) decreased in the12-d irradiation plus silymarin or Americanginseng group.3.2Western blot resultsCompared with the normal group, the mean grey level ratio of the Nrf2protein expression in the12-d irradiation group was significantly (P<0.01)increased. Compared with the12-d irradiation group, the mean grey level ratioof the Nrf2protein expression in both the12-d irradiation plus silymarin andAmerican ginseng groups was significantly (P＜0.05and P＜0.01,respectively) decreased.4Intervention effects of American ginseng on the hepatic ATM and H2AX inthe12-d irradiation groupCompared with the normal group, the mean grey level ratio of the hepatictissue ATM increased significantly (P<0.05) after irradiation with enhancedexpression. Compared with the12-d irradiation group, the mean grey levelratio of the hepatic tissue ATM in the12-d irradiation plus silymarin orAmerican ginseng group decreased significantly (P<0.05and P<0.01,respectively) with decreased expression.Compared with the normal group, the mean grey level ratio of the H2AXin the hepatic tissue in the12-d irradiation group increased significantly (P<0.05) with increased expression. Compared with the12-d irradiation group,the mean grey level ratio of the hepatic tissue H2AX in the12-d irradiationplus silymarin or American ginseng group decreased significantly (P<0.05andP <0.01, respectively) with decreased expression.5Intervention effects of American ginseng on the cell cycle and apoptosis rateof the12-d irradiation mice5.1Intervention effects of American ginseng on the cell cycleCompared with the normal group, the hepatic cells at the G0/G1stagesincreased significantly (P<0.05) after irradiation in the12-d irradiation group.Compared with the12-d irradiation group, the hepatic cells at the G0/G1stages had no significant change (P>0.05) in the12-d irradiation plus silymarin group. However, the hepatic cells at the G0/G1stages decreasedhighly significantly (P<0.01) near normal level in the12-d irradiation plusAmerican ginseng group.Compared with the normal group, the hepatic cells at S stage had nosignificant change (P>0.05) after irradiation in the12-d irradiation group.Compared with the12-d irradiation group, the hepatic cells at the S stage inthe12-d irradiation plus silymarin group decreased significantly (P<0.01)while those in the12-d irradiation plus American ginseng group had nosignificant change (P>0.05).Compared with the normal group, the hepatic cells at the G2/M stagesdecreased highly significantly (P<0.01) in the12-d irradiation group.Compared with the12-d irradiation group, the hepatic cells at the G2/M stagesin the12-d irradiation plus silymarin group had no significant (P>0.05)change while those in the12-d irradiation plus American ginseng groupincreased highly significantly (P<0.01).5.2Intervention effects of American ginseng on the hepatic apoptosis rate of12-d irradiation miceCompared with the normal group, the apoptosis rate of the hepatic cellsincreased significantly (P<0.01) after irradiation in the12-d irradiation group.Compared with the12-d irradiation group, no significant differences (P>0.05)existed in the hepatic apoptosis rate in the12-d irradiation plus silymaringroup whereas a significant decrease (P<0.01) existed in the hepatic apoptosisrate in the12-d irradiation plus American ginseng group.Conclusion：1Long-term cell phone electromagnetic irradiation is a cause of diseases,and this cause of disease is characterized as warm heat pathogen which is oneof the six external factors causing diseases. The warm heat pathogen can leadto damage to the QI YIN. The Chinese medicine, American ginseng, has thefunction of tonifying QI and YIN for the treatment of diseases caused by QIand YIN deficiency. The American ginseng capsules have an interventioneffect on the hepatic damage of the mice with12-d irradiation. 2The American ginseng capsule can improve the abnormal changes ofthe hepatic histomorphology and is related to its function to decrease theoxidative damage, the Nrf2expression in the hepatic cells, and the proteinexpression of ATM and H2AX, and to affect the cell cycle and cell apoptosis.更多还原