Baicalin treatment regulates hyperactivity of HPA axis and alters SIRT1 related inflammation in the hypothalamus in a model of depression

OBJECTIVE Hyperactivityof hypothalamic-pituitary-adrenal(HPA) axis is an important aetiological risk factor for the development of depression. Previous studies have demonstrated that the phenolic monomer baicalin has antidepressant-like effects and decreases serum corticosterone levels.However,the mechanism by which baicalin regulates hyperactivity of HPA axis remains unclear. This work aimed to investigate the effects of baicalin on hyperactivity of HPA axis using the olfactory bulbectomised(OBX) rat model of depression. METHODS Animals were anaesthetised with 10% chloral hydrate(3.3 mL·kg^(-1),ip). Using disinfected surgical equipment,the skull covering the olfactory bulbs was exposed by a midline incision. Two burr holes(2 mm diameter) were drilled 8 mm anterior to the bregma and 2 mm lateral to the midline. Both olfactory bulbs were aspirated and the holes filled with glass ionomer cement. The scalp was sutured closed. Sham-operated rats underwent every surgical procedure except the aspiration of the bulbs. The animals received penicillin(8×10~5U) intramuscularly(0.2 mL/300 g) once per day for 3 d post-surgery to prevent infection,and were subsequently housed alone in polypropylene cages. The experiments continued after 14 d of rehabilitation. The following groups were used for experiments: sham-operated(underwent surgical procedure without aspiratedolfactory bulbs and administration of vehicle only),OBX-model(underwent every surgical procedure and administration of vehicle only),OBX-amitriptyline treated(10 mg·kg^(-1)),and OBX-baicalin treatment(20 and 40 mg·kg^(-1)). Amitriptyline and baicalin were dissolved in physiological saline. RESULTS We examined how baicalin altered OBX-induced changes in serum glucocorticoid level as wel as inflammatory responses,sirtuin 1(SIRT1) expression,and p65 acetylation in the hypothalamus. Similar experiments were performed to analyse the effects of baicalin on lipopolysaccharide-induced inflammatory responses inhypothalamus. CONCLUSION Our results indicate that activation of the SIRT1 in the hypothalamus contributes to hyperactivity of HPA axis,which can be alleviated by baicalin.

坤宁颗粒治疗功能性子宫出血的实验研究

目的研究坤宁颗粒治疗功能性子宫出血的药理作用。方法用剪尾法和玻璃毛细管法测定小鼠出血时间、凝血时间;用血凝仪测定大鼠凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(FIB);采用药物建立早孕大鼠不完全流产的功能性子宫出血模型,用紫外分光光度法检测大鼠的子宫出血量,ELISA法测定血清雌二醇(E_(2))、孕酮(P)含量,HE染色观察子宫内膜的病理损伤;用全自动血液流变仪测定气滞血瘀大鼠模型全血黏度、血浆黏度。结果与空白组比较,坤宁颗粒可以明显缩短小鼠的出血时间、凝血时间及大鼠PT、APTT,升高大鼠FIB含量;与模型对照组比较,坤宁颗粒可以显著减少功能性子宫出血模型大鼠子宫出血量,升高血清E_(2)、P含量,改善子宫内膜病变;与模型组比较,坤宁颗粒可以显著降低气滞血瘀模型大鼠全血黏度和血浆黏度。结论坤宁颗粒可治疗功能性子宫出血模型大鼠子宫出血,其机制可能与调节E_(2)、P水平,改善子宫血液循环,促进子宫修复有关。

延丹胶囊对异丙肾上腺素诱导大鼠心肌缺血的作用及机制

目的研究延丹胶囊对异丙肾上腺素诱导大鼠心肌缺血损伤的改善作用及机制。方法SD大鼠随机分成空白组,模型组(40 mg/kg异丙肾上腺素),通心络胶囊组(200.57 mg/kg)及延丹胶囊低、中、高剂量组(154、308、616 mg/kg),连续灌胃给药8 d。从第6天开始,除空白组外,其余各组大鼠腹腔注射异丙肾上腺素(40 mg/kg),连续3 d,首次腹腔注射异丙肾上腺素(40 mg/kg)后,心电图监测SD大鼠心电图ST段的变化。末次腹腔注射异丙肾上腺素(40 mg/kg)后进行取材,HE染色观察心肌细胞病理损伤程度,试剂盒检测大鼠血清丙二醛(MDA)、超氧化物歧化酶(T-SOD)、谷草转氨酶(AST)、低氧诱导因子(HIF-1α)、肿瘤坏死因子(TNF-α)、白介素(IL-1β)水平,Western blot检测心肌核因子E2相关因子2(Nrf2)、血红素氧合酶1(HO-1)、抑癌基因(p53)、B淋巴细胞瘤-2基因(Bcl-2)、凋亡相关基因(Bax)蛋白表达,免疫组化检测心肌Nrf2、p53蛋白表达。结果与模型组比较,延丹胶囊能抑制SD大鼠心电图ST段抬高(P<0.05,P<0.01),改善心肌细胞病理损伤程度,降低血清MDA、AST、HIF-1α、TNF-α水平(P<0.01),升高T-SOD水平(P<0.05,P<0.01),但对血清IL-1β水平无明显影响(P>0.05)。Western blot结果显示,延丹胶囊能升高心脏组织中Nrf2、HO-1蛋白表达(P<0.05,P<0.01),降低p53蛋白表达(P<0.01),改善Bcl-2/Bax蛋白表达(P<0.01)。免疫组化结果显示,延丹胶囊能显著升高心脏组织中Nrf2蛋白表达(P<0.05),同时降低p53蛋白表达(P<0.01)。结论延丹胶囊对异丙肾上腺素诱导SD大鼠心肌缺血模型具有显著的改善作用,其作用机制为抗氧化应激反应,减少心肌炎症,改善细胞凋亡。

“高频电子线路”信息化教学方法研究

“高频电子线路”课程具有理论抽象、公式众多、电路分析复杂等特点,学生在学习过程中难以理解和掌握。因此,文章研究了结合多种信息化手段的教学思路和方法,通过虚拟仿真实验帮助学生感性地理解课程中抽象的理论分析过程;利用网络建立兴趣小组,对学习过程中出现的问题及时反馈并进行讨论和解决。这些信息化教学方法的使用,可以有效提高学生的学习效率和电路设计能力。

油气集输系统节能减排的措施

伴随着社会经济、现代化发展步伐的加快,中国对各类能源的需求量越来越大。其中,油气资源作为国民经济发展的核心能源,油气资源的开发已然成为中国社会发展的重中之重。在当前油气资源开发过程中,降低开采本身的能源消耗也是当前中国油气产业发展的重点。在实际的生产运行过程中,油气集输系统所需能耗是整个原油生产工作总能耗的35%左右,是整个原有生产和开发过程中耗能最多的环节,必须重视油气集输系统的节能减排工作。

微球LiNi_(0.8)Co_(0.1)Mn_(0.1)O_2材料的制备及在改性电解液中的电化学性能

利用共沉淀辅以高温烧结法制备了椭球形三元高镍LiNi_(0.8)Co_(0.1)Mn_(0.1)O_2(LNCM811)正极材料,并用XRD、SEM和TEM对其结构和形貌进行表征。利用CV和恒流充放电测试LNCM811在添加质量含量分别为2%(w/w)DTD(硫酸乙烯酯)、1%(w/w)MMDS(甲烷二磺酸亚甲酯)及其复合添加剂2%DTD+1%MMDS的电解液中的电化学性能,并利用EIS测试其充放电过程中的动力学特性。结果发现相较于1%MMDS,2%DTD能较为显著提高LNCM811在常温的首周放电容量和首周库伦效率;1%MMDS和2%DTD均能提高电极材料的长循环寿命,室温25℃条件下2%DTD比1%MMDS效果更显著,而高温60℃下1%MMDS比2%DTD更为明显;LNCM811正极无论在室温下还是高温下在复合添加剂的电解液中均具有最好循环性能。EIS测试表明2%DTD+1%MMDS复合添加剂能显著降低LNCM811动力学阻抗。

Protective effects of Huanglian Wendan Decoction aganist cognitive deficits and neuronal damages in rats with diabetic encephalopathy by inhibiting the release of inflammatory cytokines and repairing insulin signaling pathway in hippocampus

Huanglian Wendan decoction(HLWDD) has been used for the treatment of symptom of "Re", one of major causes in diabetes and metabolic disorders, according to the theory of traditional Chinese medicine. The present study aimed at investigating the cerebral protective effects of HLWDD on diabetic encephalopathy(DE), one of the major diabetic complications. The effects of HLWDD and metformin were analyzed in the streptozocin(STZ) + high-glucose-fat(HGF) diet-induced DE rats by gastric intubation. In the present study, the effects of HLWDD on cognition deficits were investigated after 30-day intervention at two daily dose levels(3 and 6 g·kg^(-1)). To explore the potential mechanisms underlying the effects of HLWDD, we detected the alterations of neuronal damages, inflammatory cytokines, and impaired insulin signaling pathway in hippocampus of the DE rats. Based on our results from the present study, we concluded that the protective effects of HLWDD against the cognitive deficits and neuronal damages through inhibiting the release of inflammatory cytokines and repairing insulin signaling pathway in hippocampus of the DE rats.

Ma Huang Tang ameliorates asthma though modulation of Th1/Th2 cytokines and inhibition of Th17 cells in ovalbumin-sensitized mice

AIM： Ma Huang Tang （Ephedra decoction, MHT） is a famous classical formula from Shang Han Lun by Zhang Zhongjing in the Han Dynasty. The anti-asthmatic effects of MHT and the possible mechanisms were tested. METHOD： An asthma model was established by ovalbumin （OVA）-induction in mice. A total of forty-eight mice were randomly assigned to six experimental groups： control, model, dexamethasone （2 mg·kg^-1） and MHT （5, 10, and 20 mg·kg^-1）. Airway resistance （Raw） was measured by the forced oscillation technique, histological studies were evaluated by hematoxylin and eosin （HE） staining, Thl/Th2 and Th17 cytokines were evaluated by enzyme-linked immunosorbent assay （ELISA）, and Thl7 cells were evaluated by flow cytometry （FCM）.RESULTS： This study demonstrated that MHT inhibited OVA-induced increases in Raw and eosinophil cotmt; interleukin （IL）-4 and IL-17 levels were recovered in bronchoalveolar lavage fluid, increased IFN-γ level in bronchoalveolar lavage fluid. Histological studies demonstrated that MHT substantially inhibited OVA-induced eosinophilia in lung tissue. Flow cytometry studies demonstrated that MHT substantially inhibited Thl 7 cells.CONCLUSION： These findings suggest that MHT may effectively ameliorate the progression of asthma, and could be further investigated for potential use as a therapy for patients with allergic asthma,

Anti-asthmatic effects of oxymatrine in a mouse model of allergic asthma through regulating CD40 signaling

The aim of the study was to investigate the anti-asthmatic effects of oxymatrine(OXY) and the possible underlying mechanisms.The mouse asthma model was established by ovalbumin(OVA) intraperitoneal injection.A total of fifty mice were randomly assigned to five groups:control,OVA,OVA + dexamethasone(Dex,2 mg·kg-1),and OVA + OXY(40 mg·kg-1),and OVA + OXY(80 mg·kg-1),respectively.Histological studies were conducted by the hematoxylin and eosin(HE) staining,the levels of interleukin-4(IL-4),interleukin-5(IL-5),interleukin-13,and Ig E were evaluated by enzyme-linked immunosorbent assay(ELISA),and the protein level of CD40 was analyzed by Western blotting.OXY inhibited OVA-induced increases in eosinophil count;the levels of IL-4,IL-5,Ig E,and IL-13 were recovered.It also substantially inhibited OVA-induced eosinophilia in lung tissues and the expression of CD40 protein.These findings suggest that OXY may effectively ameliorate the progression of asthma and could be explored as a possible therapy for patients with allergic asthma.

Tectorigenin inhibits the inflammation of LPS-induced acute lung injury in mice

AIM: In a previous study, the anti-inflammatory effects of tectorigenin were disclosed. In this study, the anti-inflammatory effects of tectorigenin on acute lung injury using a lipopolysaccharide(LPS)-induced acute lung injury(ALI) mouse model were investigated. METHOD: The cell-count in the bronchoalveolar lavage fluid(BALF) was measured. The animal lung edema degree was evaluated by the wet/dry weight(W/D) ratio. The superoxidase dismutase(SOD) activity and myeloperoxidase(MPO) activity was assayed using SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor-α(TNF-α), IL-1β, and IL-6 were assayed using an enzyme-linked immunosorbent assay method. Pathological changes of lung tissues were observed through HE staining. The inflammatory signal pathway related protein nuclear factor NF-κB p65 mR NA expression was measured by real-time PCR, and the protein level of NF-κB p65 was measured using Western blotting analysis. RESULTS: The data showed that treatment with the tectorigenin markedly attenuated the inflammatory cell numbers in the BALF, decreased nuclear factor NF-κB p65 mR NA level and protein level in the lungs, and improved SOD activity and inhibited MPO activity. Histological studies showed that tectorigenin substantially inhibited LPS-induced neutrophils in lung tissue compared with the model group. CONCLUSION: The results indicated that tectorigenin had a protective effect on LPS-induced ALI in mice.

基于均匀设计法评价柴胡-黄芩的配伍比例及抗抑郁机制

目的:研究柴胡-黄芩药对发挥抗抑郁功效的最佳配伍比例,探讨其可能的抗抑郁机制。方法:取柴胡、黄芩在2015年版《中国药典》中的规定用量,按照二因素七水平均匀设计表进行配伍分组。采用慢性不可预见温和应激(CUMS)方法造模,抑郁症模型小鼠灌胃给予柴胡-黄芩不同配伍比例的水煎剂,观察其对模型小鼠糖水偏好、强迫游泳、悬尾、开野等行为学试验的影响。将所得数据进行回归分析,通过回归方程求解最佳配伍比例。对优选的配伍比例进行验证,并测定小鼠脑海马环磷腺苷反应元件结合蛋白(CREB)磷酸化的水平及脑源性神经营养因子(BDNF)的表达,探讨柴胡-黄芩药对可能的抗抑郁机制。结果:与空白组小鼠相比,模型组小鼠糖水偏好率显著降低(P <0. 01),开野穿格次数显著减少(P <0. 01),强迫游泳不动时间和悬尾不动时间显著延长(P <0. 01);给予柴胡-黄芩水煎剂可增加模型小鼠的糖水偏好率(P <0. 05,P <0. 01)和穿格次数(P <0. 05,P <0. 01),缩短强迫游泳不动时间和悬尾不动时间(P <0. 05,P <0. 01)。验证试验显示,柴胡与黄芩配伍后可改善模型小鼠抑郁样行为,增加小鼠的糖水偏好率(P <0. 01),缩短强迫游泳不动时间和悬尾不动时间(P <0. 05,P <0. 01);柴胡-黄芩(1∶1)配伍组及柴胡-黄芩(8∶3)配伍组均可显著增加模型小鼠穿格次数(P <0. 05,P <0. 01);柴胡-黄芩(1∶1)配伍组在强迫游泳试验和悬尾试验中优于柴胡-黄芩(3∶8)和(8∶3)配伍组(P <0. 05,P <0. 01),在糖水偏好试验和开野试验中显著优于柴胡-黄芩(3∶8)配伍组(P <0. 05),且柴胡-黄芩(1∶1)配伍组促进海马中CREB磷酸化和增加海马中BDNF表达的效果最佳。结论:柴胡-黄芩药对可改善CUMS小鼠抑郁样行为,发挥抗抑郁功效,其最佳配伍比例为1∶1,最佳用量均约为5 g,其抗抑郁的作用机制可能与促进海马中CREB磷酸化和增加海马中BDNF表达有关。

Antidepressant-like effect of essential oil of Perilla frutescens in a chronic, unpredictable, mild stress-induced depression model mice

Perilla frutescens(Perilla leaf), a garnishing vegetable in East Asian countries, as well as a plant-based medicine, has been used for centuries to treat various conditions, including depression. Several studies have demonstrated that the essential oil of P. frutescens(EOPF) attenuated the depressive-like behavior in mice. The present study was designed to test the anti-depressant effects of EOPF and the possible mechanisms in an chronic, unpredictable, mild stress(CUMS)-induced mouse model. With the exposure to stressor once daily for five consecutive weeks, EOPF(3, 6, and 9 mg·kg-1) and a positive control drug fluoxetine(20 mg·kg-1) were administered through gastric intubation to mice once daily for three consecutive weeks from the 3rd week. Open-field test, sucrose consumption test, tail suspension test(TST), and forced swimming test(FST) were used to evaluate the behavioral activity. The contents of 5-hydroxytryptamine(5-HT) and its metabolite, 5-hydroxyindoleacetic acid(5-HIAA), in mouse hippocampus were determined by HPLC–ECD. Serum interleukin(IL)-1, IL-6, and tumor necrosis factor(TNF)-α levels were evaluated by enzyme-linked immunosorbent assay(ELISA). The results showed that CUMS significantly decreased the levels of 5-HT and 5-HIAA in the hippocampus, with an increase in plasma IL-6, IL-1β, and TNF-α levels. CUMS also reduced open-field activity, sucrose consumption, as well as increased immobility duration in FST and TST. EOPF administration could effectively reverse the alterations in the concentrations of 5-HT and 5-HIAA; reduce the IL-6, IL-1β, and TNF-α levels. Moreover, EOPF could effectively reverse alterations in immobility duration, sucrose consumption, and open-field activity. However, the effect was not dose-dependent. In conclusion, EOPF administration exhibited significant antidepressant-like effects in mice with CUMS-induced depression. The antidepressant activity of EOPF might be related to the relation between alteration of serotonergic responses and anti-inflammatory effects.

Qifu-Yin attenuates AGEs-induced Alzheimer-like pathophysiological changes through the RAGE/NF-κB pathway

Qifu-Yin(QFY), a widely used formula of traditional Chinese medicine(TCM) derived from "Jingyue Quanshu", is one of the most commonly used TCM prescriptions for the clinical treatment of Alzheimer disease. The role of advanced glycation end products(AGEs) and its receptor RAGE have attracted increasing attention as the pivotal role of Aβ has been questioned. The present study was designed to test the neuroprotective effects of QFY, and the possible mechanism in AGE-induced Alzheimer model rats. After injection of AGE in the CA3 area of the hippocampus, QFY(8.6, 4.3, and 2.15 g·kg–1), and a positive control drug donepezil(2 mg·kg–1) were administrated through gastric intubation to rats once daily for thirty consecutive days. Another positive control group was the AGE + anti-RAGE group, which was simultaneously injected with anti-RAGE antibody before AGE treatment. The control group, sham-operated group, as well as the AGE + anti-RAGE group received saline at the same dosage. The Morris water maze test and the step-down passive avoidance test were conducted to evaluate the cognitive function of the rats. The expression of RAGE and NF-κB were assayed by immunohistochemical staining. The levels of Aβ, TNF-α, and IL-1β in the hippocampus were measured by enzyme-linked immunosorbent assay(ELISA). The results showed that QFY could significantly attenuate the memory impairment induced by AGE, decrease the expressions of RAGE and NF-κB, and reduce the levels of Aβ, TNF-α, and IL-1β in the hippocampus in a dose-dependent manner. Also, the blockage of RAGE could significantly reduce the impairments caused by AGEs. In conclusion, QFY could attenuate AGEs-induced, Alzheimer-like pathophysiological changes. These neuroprotective effects might be related to the RAGE/NF-κB pathway and its anti-inflammatory activity.

Jiawei Erzhiwan improves menopausal metabolic syndrome by enhancing insulin secretion in pancreatic β cells

Menopausal metabolic syndrome(MMS) is a series of syndrome caused by ovarian function decline and hormone insufficiency, and is a high risk factor for cardiovascular diseases(CVD) and type II diabetes mellitus(T2DM). Erzhiwan(EZW),composed of Herba Ecliptae and Fructus Ligustri Lucidi, is a traditional Chinese herbal formula that has been used to treat menopausal syndrome for many years. We added Herba Epimedii, Radix Rehmanniae, and Fructus Corni into EZW, to prepare a new formula, termed Jiawei Erzhiwan(JE). The present study was designed to determine the anti-MMS effects of JE using ovariectomized(OVX) adult female rats that were treated with JE for 4 weeks, and β-tc-6 cells and INS cells were used to detected the protect effectiveness of JE. Our results showed JE could increase insulin sensitivity and ameliorated hyperlipidemia. Metabolomics analysis showed that the serum levels of branched and aromatic amino acids were down-regulated in serum by JE administration. Moreover, JE enhanced the function of islet βcells INS-1 and β-tc-6, through increasing the glucose stimulated insulin secretion(GSIS), which was abolished by estrogen receptor(ER)antagonist, indicating that JE functions were mediated by ER signaling. Additionally, JE did not induce tumorigenesis in rat mammary tissue or promoted proliferation of MCF-7 and Hela cells. In conclusion, our work demonstrated that JE ameliorated OVX-induced glucose and lipid metabolism disorder through activating estrogen receptor pathway and promoting GSIS in islet β cells, thus indicating that JE could be a safe and effective medication for MMS therapy.