目的 探究基于高迁移率族蛋白(HMG)B1/Toll样受体(TLR)4 信号通路使用迷走神经刺激(VNS)治疗难治性癫痫大鼠的效果.方法 将 40 只大鼠随机分为空白对照组(A组)、难治性癫痫模型组(B组)、假刺激组(C组)、VNS组(D组)每组各 10 只.A组、B组不作任何刺激处理,C组左颈部植入VNS电极,但不刺激通电.D组左颈部植入VNS电极进行通电刺激.对比分析各组海马CA3 区状况、每周癫痫发作次数、海马组织存活锥体细胞数、阳性细胞数、海马区单核趋化蛋白(MCP)-1、层黏连蛋白(LAP)、P糖蛋白(P-gp)灰度比值,HMGB1、TLR4 蛋白表达.结果 与A组相比,B组、C组海马CA3区细胞数量最少,且出现形态的严重损伤,核仁溶解、缩小、模糊不清,核断裂现象严重;D组海马CA3 区细胞数量大幅度增加、形态趋于正常,核仁状态恢复良好.刺激结束 1 w后,与B、C组相比,D组刺激结束后癫痫发作频率显著减少(P＜0.05).与A组相比,B组、C组海马组织存活锥体细胞数明显减少、海马组织阳性细胞数明显增加(P＜0.05),与B、C组比较,D组海马组织存活锥体细胞数明显增加,海马组织阳性细胞数明显减少(P＜0.05).与A组相比,B组、C组海马区MCP-1、LAP、P-gp灰度比值、HMGB1、TLR4 表达明显增加(P＜0.05);与B、C组比较,D组海马区MCP-1、LAP、P-gp灰度比值、HMGB1、TLR4 表达明显降低(P＜0.05).结论 VNS可抑制难治性癫痫的发作,保护海马神经元,调节癫痫大鼠海马CA3 区的基因表达;同时,通过抑制HMGB1/TLR4 信号通路活性逆转耐药基因,进而调节神经功能,为难治性癫痫的治疗提供了新方向.

目的 探讨迷走神经刺激(VNS)对难治性癫痫大鼠认知功能的影响及可能机制.方法 通过腹腔注射氯化锂-皮罗卡品建立难治性癫痫大鼠模型.模型制作成功大鼠随机分为模型组(18只)与VNS组(15只),另外设对照组(20只).对照组与模型组只分离迷走神经并植入刺激器,但不给予刺激;VNS组采取连续4周迷走神经电刺激.观察大鼠癫痫发作情况;Morris水迷宫实验检测大鼠认知功能;Nissl染色观察大鼠海马组织病理形态;ELISA检测大鼠海马组织TNF-α、IL-6和IL-10表达;免疫荧光染色法与Western-blot分别检测大鼠海马组织M1型小胶质细胞标记物(iNOS)和M2型小胶质细胞标记物(Arg1)相对表达.结果 ①与对照组相比,模型组大鼠癫痫发作等级及发作持续时间明显增加(P＜0.05);通过VNS连续干预4周后,大鼠癫痫发作等级及发作持续时间明显降低(P＜0.05).②模型组大鼠逃避潜伏期时间明显长于对照组,而穿越原平台的次数明显少于对照组(P＜0.05);通过VNS连续干预4周后,癫痫大鼠逃避潜伏期时间明显缩短,而穿越原平台的次数明显增加(P＜0.05).③对照组大鼠海马神经元形态正常;模型组大鼠海马神经元损伤严重,数量明显减少(P＜0.05);VNS组大鼠海马神经元损伤相比模型组明显减轻,数量明显增加(P＜0.05).④模型组大鼠海马组织TNF-α、IL-6相对表达明显高于对照组,而IL-10相对表达明显降低(P＜0.05);通过VNS连续干预4周后,癫痫大鼠海马组织TNF-α、IL-6相对表达明显降低,而IL-10相对表达明显增加(P＜0.05).⑤与对照组相比,模型组大鼠海马组织iNOS相对表达明显增加,而Arg1相对表达明显减少(P＜0.05);与模型组相比,VNS组大鼠海马组织iNOS相对表达明显减少,而Arg1相对表达明显增加(P＜0.05).结论 VNS具有改善难治性癫痫大鼠认知功能障碍的作用,其机制可能是通过促进M2型小胶质细胞极化,减轻中枢炎性反应,保护海马神经元.

目的 研究特异性α7烟碱型乙酰胆碱受体(α7nAChR)激动剂PNU-282987对颞叶癫痫(TLE)模型大鼠认知功能的影响及机制.方法 将60只大鼠随机分为对照组、模型组、PNU-282987组(3 mg/kg)和甲基牛扁亭(MLA)+PNU-282987组(6 mg/kg MLA+3 mg/kg PNU-282987),每组15只.除对照组之外,其余各组大鼠均制备TLE模型.造模成功后,各组大鼠腹腔注射相应药物或生理盐水,每天1次,连续2周.观察大鼠癫痫发作行为并进行评分,记录发作持续时间;检测大鼠认知功能;观察海马组织CA1区神经元病理学形态;检测海马组织中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和IL-1β水平;检测海马组织中离子钙接头蛋白1(IBA-1)阳性表达和α7nAChR、核因子κB(NF-κB)p65、磷酸化NF-κB p65(p-NF-κB p65)蛋白表达水平.结果 与模型组比较,PNU-282987组大鼠癫痫评分和发作持续时间,海马组织中IBA-1阳性细胞数量和TNF-α、IL-6、IL-1β水平以及NF-κB p65、p-NF-κB p65蛋白表达水平均显著减少/降低(P＜0.05);逃避潜伏期时间显著缩短(P＜0.05),原平台象限停留时间及穿越平台次数均显著增加(P＜0.05);海马组织CA1区神经元损伤明显减轻;海马组织中α7nAChR蛋白表达水平显著升高(P＜0.05).与PNU-282987组比较,MLA+PNU-282987组大鼠上述指标均显著逆转(P＜0.05).结论 PNU-282987可改善TLE模型大鼠的认知功能障碍,其机制可能是通过激活α7nAChR/NF-κB信号通路,抑制小胶质细胞介导的炎症反应,进而减轻海马神经元损伤.

Objective: To investigate the effects of vagus nerve stimulation(VNS) on hippocampal neuro-inflammatory and α7 nicotinic acetylcholine receptor (α7nAChR) expression in rats with intractable epilepsy (IE). Methods: Eighty adult male SD rats (SPF) were randomly divided into control group, model group, VNS group and MLA+VNS group. There were respectively 20 rats in the control group and MLA+VNS group, and because of model failure and animal death, 15 rats and 14 rats in the model group and VNS group were left respectively . Except the control group, the IE model was established in other groups. Only the vagus nerve was isolated in the control group without electrical stimulation; the model group did not take any intervention measures; the VNS group was treated for 4 weeks with VNS after the model was successful; the MLA(3.4 μg/μl, 5 μl) was given to the lateral ventricle in the MLA+VNS group, and then VNS for 4 weeks. Seizure frequency and duration in each group were observed and recorded. And then the rats were decapitated, the hippocampus were quickly separated and 10% tissue homogenate was prepared. The homogenate was centrifuged and the supernatant was extracted. The activities of AChE and ChAT in the supernatant were measured by spectrophotometry, and the levels of TNF-ɑ, IL-6 and IL-1β were detected by ELISA. The expression of α7nAChR in rat hippocampals was detected by Western blot. The expression of α7nAChR on microglias in rat hippocampals was assesed by double-labeled immunofluorescence. Results: ①After VNS for 4 weeks, the frequency and duration of seizures in rats were decreased significantly, which were lower than those of the model group (P<0.01); After treated with MLA +VNS, the frequency and duration of seizures in rats were also reduced significantly, which were lower than those of the model group, but higher than those of the VNS group (P<0.01).②Compared with the control group, the expression of ChAT in the hippocampus of rats in the model group was decreased significantly and the expression of AChE was increased significantly (P<0.01); Compared with the model group, the expressions of ChAT in the hippocampus of rats in the VNS group and MLA+VNS group were increased significantly and the expressions of AChE were decreased significantly (P<0.01); Compared with the VNS group, in the hippocampus of rats in the MLA+VNS group, the expressions of ChAT and AChE had no significant changes (P>0.05). ③Compared with the control group, the expressions of TNF-ɑ, IL-6 and IL-1β in the hippocampus of rats in the model group were increased significantly (P<0.01). Compared with the model group, the expressions of TNF-ɑ, IL-6 and IL-1β in the hippocampus of rats in the VNS group were decreased significantly (P<0.01). Compared with the VNS group, the expressions of TNF-ɑ, IL-6 and IL-1β in the hippocampus of rats in the MLA+VNS group were increased significantly(P<0.01). ④Compared with the control group, the expression of α7nAChR in hippocampus and microglia of rats in the model group was decreased significantly(P<0.01); Compared with the model group, the expression of α7nAChR in hippocampus and microglia of rats in the VNS group was up-regulated significantly (P<0.01); Compared with the VNS group, coexpression of α7nAChR on microglia wasreduced significantly in the MLA+VNS group (P<0.01). Conclusion: VNS has obvious therapeutic effect on IE rats, and its mechanism may be related to activating hippocampal microglia cholinergic anti-inflammatory pathway directly and inhibiting hippocampal neuro-inflammatory response.

Objective: To analyse the effect of glycyrrhizin (GL) on kainic acid (KA)-induced hippocampal pathological damage through the HMGB1/TLR4/P-NF-kappa B pathway. Methods: Sixty male 21-day-old Sprague Dawley (SD) rats were randomly divided into a control group, a KA group, and a GL group. The control group was injected intraperitoneally with normal saline, the KA group was injected with KA, and the GL group was injected intraperitoneally with KA. The SE and death of mice were observed after modelling, and the time when rats reached grade III attack (SOT) was recorded. After seven days of modelling, the mice were killed, the pathological changes were observed by HE staining, and the expression of the neuronal antinuclear antibody (Neu-N) was detected. RT-PCR was used to detect the expression of HMGB1 and TLR-4 mRNA, and Western blot was used to detect the protein expression of HMGB1, TLR4, and P-NF-kappa B. Results: The incidence of SE and mortality in the GL group were 50.00% and 10.00%, respectively, significantly lower than 80.00% and 40.00% of the KA group. Furthermore, the level of SOT in the GL group was significantly higher than in the KA group (P<0.05). The results of HE staining showed that the inclusion bodies of nerve cells in the KA group were shrunk and crimson, the nucleus pyknosis was noticeable, the intercellular space was enlarged, the structure was disordered, some nerve cells were lysed, and the nucleus was dissolved. Nerve degeneration and necrosis were also found in the GL group but with less severity than in the KA group. The number of Neu-N positive cells in the control and GL groups were significantly higher than in the KA group (P<0.05). The HMGB1 and TLR-4 mRNA expression levels were significantly higher in the KA group than in the control and GL groups (P<0.05). The expression levels of TLR-4 and P-NF-kappa B protein in the KA group were significantly higher than those in the control and GL groups (P<0.05). Conclusion: GL can slow down KA-induced epilepsy in young rats, inhibit the pathological damage of the hippocampus, and decrease Neu-N positive cells. The mechanism may be related to GL's regulation of the HMGB1/TLR4/P-NF-kappa B pathway.

OBJECTIVE:To detect the expression level of suppressors of cytokine signaling 3 （SOCS3） in acute lymphoblastic leukemia (ALL), and to observe the effect of over-expresson of SOCS3 in Jurkat cells on the cytotoxicity of NK cells.METHODS:The expression levels of SOCS3 mRNA in peripheral blood mononuclear cells of 20 children with ALL and 20 healthy children (normal control group) were detected by RT-PCR. The peripheral blood NK cells from healthy subjects were selected by immunomagnetic technique, and the purity was detected by flow cytometry. SOCS3 was overexpressed in Jurkat cells infected with lentivirus vector, and SOCS3 mRNA expression was detected by RT-PCR after lentivirus infection. The NK cells were co-cultured with the infected Jurkat, and LDH release method was used to detect the cytotoxicity of NK cells on the infected Jurkat cells. The concentrations of TNF-α and IFN-γ were determined by ELISA. The expression of NKG2D ligands MICA and MICB on the surface of Jurkat cells were detected by flow cytometry. Western blot was used to detect the effect of SOCS3 overexpression on STAT3 phosphorylation in Jurkat cells.RESULTS:Compared with the control group, the mRNA expression of SOCS3 in the peripheral blood mononucleated cells of ALL children was significantly decreased. The purity of NK cells isolated by flow cytometry could reach more than 70%. The expression of SOCS3 mRNA in Jurkat cells increased significantly after lentivirus infection. Overexpression of SOCS3 in Jurkat cells significantly promoted the killing ability of NK cells and up-regulated the secretion of TNF-α and IFN-γ from NK cells. The results of flow cytometry showed that the expression of NKG2D ligands MICA and MICB on Jurkat cells increased significantly after SOCS3 overexpression. Western blot results showed that overexpression of SOCS3 significantly reduced the phosphorylation level of STAT3 protein in Jurkat cells.CONCLUSION:SOCS3 mRNA expression was significantly decreased in ALL patients, and overexpression of SOCS3 may up-regulate the expression of MICA and MICB of NKG2D ligands on Jurkat cell surface through negative regulation of JAK/STAT signaling pathway, thereby promoting the cytotoxic function of NK cells.

目的 探究微小RNA(miR)-199a-3p调控非受体酪氨酸激酶(JAK)信号转导和转录激活因子3(STAT3)通路对心力衰竭(HF)大鼠模型心脏功能的影响和机制.方法 30只建模成功的大鼠随机分为HF+miR-199a-3p组和HF组(n=15),选取15只正常大鼠作为对照组.HF+miR-199a-3p组尾静脉注射miR-199a-3p类似物.检测各组miR-199a-3p、心肌细胞凋亡指数、炎性因子白细胞介素6(IL-6)、TNF-α、JAK和STAT3蛋白表达水平.结果 HF组miR-199a-3p表达明显低于对照组,心肌细胞凋亡指数、IL-6、TNF-α、JAK及STAT3蛋白表达明显高于对照组(P＜0.05).HF+miR-199a-3p组miR-199a-3p明显高于HF组,心肌细胞凋亡指数、IL-6、TNF-α、JAK2和STAT3蛋白水平明显低于HF组,有统计学差异[1.67±0.11vs0.41±0.05,(13.62±1.47)％vs(28.34±2.75)％,(26.73±3.17)ng/L vs(38.21±4.09)ng/L,(25.56±2.98)ng/L vs(47.24±5.11)ng/L,1.82±0.16vs 3.65±0.31,2.04±0.17vs3.89±0.33,P＜0.05].结论 miR-199a-3p 通过抑制 JAK/STAT 通路缓解炎性反应抑制心肌细胞的凋亡,从而提高HF大鼠心功能.

人体解剖生理学是中药学专业的一门重要的必修课程,其中实验教学在人体解剖生理学中占有非常重要的地位,但传统的实验教学体系已经不能满足当前高等教育的需要,本文结合专科院校中药学专业人体解剖生理学改革的实际,探索新型人体解剖生理学实验教学体系,取得显著成效.

随着高等教育的发展,传统人体解剖生理学的实验教学模式已经表现出众多弊端,故对其实验教学模式从实验教学内容、实验教学方法、实验考核的评价体系进行改革探索,以期在医学专科院校中构建崭新的人体解剖生理学实验教学模式,从而充分调动学生学习的积极性,培养其创新性,独立分析问题和解决问题的能力,提高实验教学的效果.

目的 探讨香菇多糖(Lentinan,LNT)对肝癌细胞HepG2增殖的影响及机制.方法 体外培养肝癌细胞系HepG2分别给予不同浓度LNT处理,MTT法检测肝癌细胞增殖抑制率的变化,western-blot检测轴突导向蛋白4C(Sema4C)和G蛋白偶联受体激酶相互作用蛋白1(GIT1)表达.结果 不同浓度LNT作用肝癌细胞24、48、72 h后,肝癌细胞增殖的抑制率呈现浓度和时间依赖性;western-blot检测发现100μg/ml香菇多糖处理肝癌细胞48 h后,Sema4C和GIT1表达明显低于对照组(P<0.05).结论 LNT能够抑制肝癌细胞增殖,其机制可能是通过下调Sema4C和GIT1蛋白表达.

目的 探讨电刺激大鼠右侧尾壳核诱导皮层脑电高频振荡(HFO)功率谱特征.方法 实验共用雄性SD大鼠56只,体质量150?250 g,氨基甲酸乙酯麻醉下行气管插管和开颅术.将一根双极不锈钢同芯刺激电极植于右侧尾壳核,重复施加电刺激(60 Hz,2 s,0.4?0.6 mA);将两个不锈钢螺丝钉旋入双侧皮层的颅骨内,一个不锈钢螺丝钉电极旋人小脑皮层表面的颅骨内,记录双侧皮层脑电,分析脑电HFO的功率谱特征.结果 重复施加电刺激诱导出现持续时间长达近10 ms的HFO,其电活动模式呈现逐渐增大和减小的变化趋势;从功率谱上分析,显示其带宽范围为80?450 Hz,且施加刺激对侧HFO持续时间延长、振幅增强,潜伏期缩短.结论 电刺激大鼠右侧尾壳核可以诱导出现双侧皮层HFO,对侧易感,形成尾壳核一皮层癫痫网络.

目的 探讨香菇多糖(Lentinan,LNT)对癫痫模型大鼠学习记忆能力的影响以及可能的机制.方法 选取60只雄性SD大鼠,随机分为对照组、模型组、LNT干预组,各组20只.除对照组不建立癫痫模型以外,模型组与LNT干预组分别建立癫痫模型,对照组与模型组给予常规饲养,LNT干预组采用60 mg/kg LNT灌胃,持续灌胃30 d.Morris水迷宫检测各组大鼠学习记忆能力;酶联免疫法(ELISA)检测所有大鼠海马组织中TNF-α、IL-6和IL-1β含量.结果 Morris水迷宫实验结果 :与对照组比较,模型组大鼠学习记忆能力明显下降(P<0.05);与模型组比较,LNT干预组大鼠学习记忆能力明显升高(P<0.05).ELISA实验结果 :模型组大鼠海马组织TNF-α、IL-6和IL-1β含量明显高于对照组,差异有统计学意义(P<0.05);LNT干预组大鼠海马组织TNF-α、IL-6和IL-1β含量明显低于模型组,差异有统计学意义(P<0.05).结论 LNT具有提高癫痫模型大鼠学习记忆能力的作用,其机制可能是通过抑制炎症反应.

目的 研究番茄红素(LYC)对癫痫大鼠学习记忆能力的影响及抗氧化作用.方法 将60只雄性SD大鼠随机平均分为3组:空白对照组、模型组与LYC干预组.空白对照组不复制癫痫模型,常规饲养;模型组复制癲痫模型,常规饲养;LYC干预组在复制癲痫模型后,采用10 mg/kg LYC灌胃,连续灌胃28 d.28 d后所有大鼠行morris水迷宫测试.测试结束后断头处死大鼠,分离大鼠海马组织,测定海马组织内超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-PX)含量;脑组织石蜡切片,HE染色,显微镜下观察海马神经元结构.结果 水迷宫实验中,定位航行实验结果显示,与空白对照组比较,连续4 d模型组逃避潜伏期的时间明显延长,差异有统计学意义(t1=6.04,P＜0.001,t2=7.97,P＜0.001;t3=9.43,P＜0.001;t4=10.12,P＜0.001);而与模型组比较,LYC干预组连续4 d逃避潜伏期的时间缩短,差异有统计学意义(t1=3.25,P=0.002;t2=4.58,P＜0.001;t3=7.31,P＜0.001;t4=8.72,P＜0.001).空间探索实验结果显示,与空白对照组比较,模型组目标象限停留时间与穿越平台的次数均明显减少,差异有统计学意义(t次数=16.29,P＜0.001;t时间=10.35,P＜0.001);而与模型组比较,LYC干预组目标平台象限停留时间与穿越平台的次数均明显增加,差异有统计学意义(t次数=13.78,P＜0.001;t时间=7.07,PP＜0.001).与空白对照组比较,模型组大鼠海马组织SOD和GSH-PX含量明显减少,而MDA含量明显升高,差异有统计学意义(tSOD=12.37,P＜0.001;tGSH-PX=12.42,P＜0.001;tMDA=9.73,P＜0.001);与模型组比较,LYC干预组大鼠海马组织SOD和GSH-PX含量明显升高,而MDA 含量明显降低,差异有统计学意义(tSOD=3.06,P=0.004;tGSH-PX=3.30,P=0.002;tMDA=6.32,P＜0.001).HE染色结果显示,空白对照组海马神经元形态正常;模型组海马神经元数量明显减少,排列疏松和紊乱,细胞核溶解和破裂;LYC干预组海马神经元数量较模型组增多,细胞形态恢复.结论 LYC通过抗氧化应激保护海马神经元,提高癫痫大鼠学习记忆水平.

目的 探讨细菌脓毒症所致免疫麻痹中脂多糖(LPS)调控树突状细胞(DCs)免疫共抑制分子PD-L1表达的潜在机制.方法 采用流式细胞术、免疫荧光技术检测细菌脂多糖对树突状细胞PD-L1表达的影响.采用BrdU细胞增殖实验和γ-干扰素酶联免疫斑点实验分别检测脂多糖所致树突状细胞PD-L1表达对抗原特异性T细胞增殖反应及细胞毒性T细胞反应的影响.通过PD-L1封闭抗体和PI3K抑制剂LY294002分别探究PD-L1分子和PI3K-Akt信号在细菌LPS调控树突状细胞(DCs)免疫麻痹中的作用.结果 LPS显著上调DCs免疫共抑制分子PD-L1表达,并抑制DCs介导的T淋巴细胞免疫反应(P＜0.0001).LPS显著激活DCs的PI3K和AKT信号.PI3K抑制剂LY294002显著降低LPS所致PD-L1的高水平表达.PD-L1封闭抗体和抑制剂LY294002均能显著逆转细菌内毒素LPS诱导的DCs抗原特异性T淋巴细胞免疫反应的抑制现象(P＜0.000 1).结论 细菌脂多糖所致树突状细胞免疫共抑制分子PD-L1的高表达引起细菌脓毒症中T细胞免疫反应低下的麻痹现象.阻断PD-L1或阻断PI3K-AKT信号有助于改善脂多糖所致PD-L1高表达介导的树突状细胞免疫麻痹.

目的:研究枸杞多糖(lycium barbarum polysaccharides,LBP)对癫痫大鼠学习记忆能力的影响及其抗氧化应激作用.方法:将雄性SD大鼠60只随机分为正常对照组、癫痫模型组、LBP干预组,各组20只.正常对照组采取常规饲养,不建立癫痫模型;采用经典氯化锂-匹鲁卡品方法建立癫痫模型,模型组模成模后采取常规饲养;LBP干预组在建立癫痫模型后,采用50 mg/kg LBP灌胃,持续灌胃14 d.14 d后,分别对3组大鼠行morris水迷宫测试.测试完成后,取海马组织,测定海马组织内超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-PX)含量.结果:1)与正常对照组比较,模型组大鼠逃避潜伏期时间明显延长(T1 =7.72,T2 =8.73,T3=9.92,T4 =11.88;P=0.00);与模型组比较,LBP组大鼠逃避潜伏期时间明显缩短(T1=5.75,T2=5.91,T3=7.80,T4 =6.97,P=0.00).与正常对照组比较,模型组大鼠平台象限路径百分比与平台象限停留时间明显缩短(T1=15.05,P=0.00;T2=7.62,P=0.00);与模型组比较,LBP组大鼠平台象限路径百分比与平台象限停留时间明显延长(T1 =7.62,P=0.00;T2=2.47,P=0.02).2)与正常对照组比较,模型组大鼠海马组织SOD、GSH-PX含量明显降低(TSOD=10.16,P=0.00;TGSH =9.03,P=0.00),MDA含量明显升高(T=6.43,P＜0.01);与模型组比较,LBP干预组大鼠SOD、GSH-PX含量明显升高(TSOD=4.13,P=0.00;TGSH=5.58,P=0.00),MDA含量明显降低(T=2.50,P=0.02).结论:LBP能够提高癫痫大鼠学习记忆能力,其机制可能与通过增强抗氧化应激作用保护海马神经元细胞有关.

目的 癫痫是因脑部神经元异常放电所导致的中枢神经功能障碍的临床综合征,长期反复发作会导致学习记忆能力的下降.本研究探讨枸杞多糖(lycium barbarum polysaccharides,LBP)对癫痫大鼠学习记忆能力影响及其可能机制.方法 将雄性SD大鼠60只随机分为对照组、癫痫模型组和LBP干预组,每组20只.对照组采取常规饲养,不建立癫痫模型;模型组建立癫痫模型,每天灌胃等量生理盐水;LBP干预组在建立癫痫模型后,采用50 mg/kg LBP灌胃.持续灌胃14 d.14 d后,3组大鼠行Morris水迷宫测试.水迷宫实验结束后,处死大鼠取海马组织,酶联免疫法测肿瘤坏死因子-α (tumor necrosis factor-α,TNF-α)、白介素-6(interleukin,IL-6)和白介素-1β(interleukin-1β,IL-1β)含量.结果 水迷宫定位航行实验结果显示,模型组大鼠逃避潜伏期长于LBP干预组和对照组,差异有统计学意义,均P＜0.001.空间探索实验结果显示,模型组大鼠平台象限路径百分比低于LBP干预组和对照组,差异有统计学意义,F=101.50,P＜0.001;平台象限停留时间短于LBP干预组和对照组,差异有统计学意义,F=32.51,P＜0.001.模型组大鼠海马组织TNF-α含量(F=22.28,P＜0.001)、IL-1β含量(F=61.07,P＜0.001)和IL-6含量(F=19.91,P＜0.001)高于LBP干预组和对照组,差异有统计学意义.结论 LBP能够提高癫痫大鼠学习记忆能力水平,其机制可能是通过抗感染作用实现的.

目的:研究山茱萸多糖对癫痫大鼠学习记忆能力的影响及其可能机制.方法:将雄性SD大鼠30只随机分为对照组、 癫痫模型组、 山茱萸多糖干预组,各组10只.对照组采取常规饲养,不建立癫痫模型;模型组建立癫痫模型,常规饲养;山茱萸多糖干预组在建立癫痫模型后,采用0.28 g/kg山茱萸多糖灌胃,持续灌胃14 d.14 d后分别对3组大鼠行morris水迷宫测试.测试完成后,取海马组织,测定海马组织内SOD、MDA和GSH-PX含量.结果:与对照组比较,模型组大鼠逃避潜伏期时间明显延长(P<0.05);与模型组比较,山茱萸多糖干预组大鼠逃避潜伏期时间明显缩短(P<0.05).与对照组比较,模型组大鼠平台象限路径百分比与平台象限停留时间明显缩短(P<0.05);与模型组比较,山茱萸多糖干预组大鼠平台象限路径百分比与平台象限停留时间明显延长(P<0.05).与对照组比较,模型组大鼠海马组织SOD、GSH-PX含量明显降低(P<0.05),MDA含量明显升高(P<0.05);与模型组比较,山茱萸多糖干预组大鼠SOD、GSH-PX含量明显升高(P<0.05),MDA含量明显降低(P<0.05).结论:山茱萸多糖具有提高癫痫大鼠学习记忆能力的作用,其机制可能是通过抗氧化作用来实现的.

目的:探讨香菇多糖对人肝癌HepG2、Huh7.5.1细胞体外侵袭的影响及其机制.方法:分别以0(空白对照组)、100μg/mL香菇多糖作用肝癌细胞48h,采用Transwell侵袭实验考察其对细胞侵袭的影响;采用实时荧光定量聚合酶链式反应法(Real time Quantitative PCR,qRT-PCR)考察miRNA-138表达改变.结果:100μg/mL香菇多糖作用肝癌细胞48h后,肝癌HepG2、Huh7.5.1细胞体外侵袭能力明显抑制,细胞中miR-138表达明显升高,较空白对照组差异均有统计学意义(P<0.05);其中香菇多糖对人肝癌Huh7.5.1细胞作用更明显(P<0.05).结论:香菇多糖可抑制人肝癌HepG2、Huh7.5.1细胞体外侵袭,其机制可能通过上调miR-138表达.

目的:探讨香菇多糖对肝癌细胞Huh7.5.1增殖的影响及其机制.方法:采用MTT法检测6.25,12.5,25,50,100 mg/L香菇多糖分别作用肝癌细胞24,48,72 h后,肝癌细胞增殖抑制率变化;qRT-PCR检测100 mg/L香菇多糖处理肝癌细胞48 h后,微小RNA138(miR-138)表达变化.结果:细胞的增殖抑制率随香菇多糖质量分数的增高、作用时间的延长呈依赖性升高;相同作用时间,12.5,25,50,100 mg/L香菇多糖组的细胞增殖抑制率较6.25 mg/L组明显升高,差别有统计学意义(P ＜0.05或P＜0.01);相同质量分数的香菇多糖组48 h、72 h的细胞增殖抑制率较同组内24 h明显升高,差别有统计学意义(P＜0.05或P＜0.01);100 mg/L香菇多糖作用48 h后肝癌细胞抑制率为(50.36±5.13)％,作为后续实验质量分数和作用时间.qRT-PCR检测发现,100 mg/L香菇多糖处理肝癌细胞48 h后,miR-138表达明显高于对照组,差别有统计学意义(P＜0.05).结论:香菇多糖能够抑制肝癌细胞增殖,可能是通过提高肝癌细胞miR-138表达实现的.

目的:探讨香菇多糖对肝癌细胞Huh7.5.1增殖和侵袭的影响.方法:采用MTT法检测6.25、12.5、25、50、100μg/mL香菇多糖分别作用肝癌细胞24、48、72 h后,肝癌细胞增殖抑制率变化;采用Transwell侵袭实验考察其对细胞侵袭的影响.结果:6.25、12.5、25、50、100μg/mL香菇多糖分别作用肝癌细胞24、48、72h后,细胞的抑制率呈浓度和时间依赖性升高,100μg/mL香菇多糖作用48 h后肝癌细胞抑制率为(50.36±5.13)％,作为后续实验浓度和作用时间;100μg/mL香菇多糖处理肝癌细胞48 h后,肝癌HepG2细胞体外侵袭能力明显抑制(P＜0.05).结论:香菇多糖能够抑制肝癌细胞增殖和侵袭.