桑黄多糖抗疲劳及耐缺氧实验研究

研究采用水提醇沉法得到桑黄菌丝多糖(大分子量粗多糖),通过小鼠抗疲劳、耐缺氧能力实验,研究桑黄菌丝多糖的生理活性。以小鼠游泳力竭时间、游泳前后血乳酸、肝糖原以及血清尿素氮含量的变化为指标,考察桑黄多糖抗疲劳能力,以小鼠在缺氧和亚硝酸钠中毒环境下的存活时间为指标,考察桑黄多糖耐缺氧能力。结果表明,灌胃桑黄多糖可以显著延长小鼠游泳时间达70.62%,降低游泳后乳酸曲线下面积22.89%,提高肝糖原储备33.36%,减少游泳后血清尿素氮含量23.17%,延长小鼠在缺氧环境下42.08%和亚硝酸钠中毒环境下35.29%的存活时间。因此,桑黄多糖具有提高小鼠抗疲劳和耐缺氧能力的作用,且在一定剂量范围内,实验效果与灌胃剂量呈正效应关系。     

冬虫夏草固体发酵物水提液抗疲劳作用初步研究

通过研究冬虫夏草(Ophiocordyceps sinensis)固体发酵物水提液对负重小鼠游泳时间的影响,初步探讨其抗疲劳作用。结果表明:与阴性对照组相比,灌胃喂养冬虫夏草固体发酵物水提液的小鼠负重游泳时间显著延长,证明在本试验条件下冬虫夏草固体发酵物具有显著的抗疲劳作用。     

食(药)用菌抗疲劳作用实验研究

将香菇和灰树花2种食（药）用菌的菌种分别接种到灵芝渣和云芝渣上（提取下脚料）,进行固体发酵,然后与全灵芝破壁孢子粉分别采用超声波水提法和醇提法制备提取物,通过小鼠灌胃20d-30d后进行负重游泳实验,初步评价和验证上述提取物的抗疲劳作用。试验结果表明：香菇固体发酵物的醇提液、灰树花固体发酵物及全灵芝破壁孢子粉水提物组小鼠的负重游泳时间比对照组显著延长（P〈0.05）;提示上述提取物具有抗疲劳作用。     

枇杷叶多糖对小鼠抗疲劳能力的影响

以热水提取枇杷叶中的水溶性多糖,用灌胃方法研究了枇杷叶多糖对小鼠抗疲劳能力的影响。结果显示,服用枇杷叶多糖小鼠的游泳时间比对照组小鼠延长了37.4%。从而证实枇杷叶多糖是枇杷叶的功能成分之一,能明显提高小鼠的抗疲劳能力。     

桑黄胞内多糖抗衰老作用的研究

研究了桑黄胞内多糖（PHPS）对果蝇寿命的影响和对D-半乳糖致小鼠衰老模型的抗衰老作用，结果表明。PHPS能延长果蝇平均寿命和最长寿命．提高衰老小鼠血清、脑、肝组织中超氧化歧化酶（SOD）活性．降低小鼠血清、脑、肝组织中丙二醛（MDA）的含量．增加胸腺的重量和改善小鼠学习记忆行为。说明PHPS具有一定的抗衰老、抗氧化作用。     

皱环球盖菇抗疲劳作用活性部位筛选

为了探讨和筛选皱环球盖菇(Stropharia rugosoannulata)抗疲劳作用和活性部位,将160只昆明种小鼠分为2批,每批8组(80%乙醇提取物、石油醚萃取物、氯仿萃取物、乙酸乙酯萃取物、正丁醇萃取物、水层、阳性对照和空白对照组),每组10只,以红景天胶囊为阳性对照,每日灌胃1次,给药30 d。一批小鼠用来观察记录负重力竭游泳时间;另一批小鼠游泳30 min后,摘除眼球取血测定血清中尿素氮(blood urea nitrogen,BUN)、乳酸(lactic acid,LA)、乳酸脱氢酶(lactate dehydrogenase,LDH)、肌酸激酶(creatine kinase,CK)的值;取血后摘出左后肢股四头肌和肝脏,计算肝脏系数,分别测定左后肢股四头肌中肌糖原(muscle glycogen,MG)含量与肝脏中肝糖原(liver glycogen,LG)、超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)的值。结果表明:皱环球盖菇氯仿萃取物提高了52.93%的小鼠负重力竭游泳时间,也可明显提高LDH和SOD活力,提高肌肉组织与肝脏中糖原含量,小鼠体内LG含量达(11. 10±1.41) mg/g,运动后BUN、LA、CK、MDA水平不同程度下降,小鼠肝脏中MDA含量与空白对照组相比下降17.58%。皱环球盖菇具有抗疲劳作用,发挥抗疲劳作用的活性成分主要分布于氯仿分部。     

灵芝提取物及复合制剂改善睡眠和免疫调节的研究

目的：研究灵芝提取物及复合制剂改善睡眠和免疫调节的作用；方法：小鼠给予灵芝提取物及复合制剂30d后，通过直接睡眠试验、延长戊巴比妥钠睡眠时间、戊巴比妥钠阈下催眠剂量试验和缩短巴比妥钠睡眠潜伏期试验评价改善睡眠作用；通过DNFB诱导的小鼠迟发性变态反应（DTH）和碳廓清试验观察免疫调节的作用；结果：与对照组相比，灵芝提取物及复合制剂能显著延长戊巴比妥钠睡眠时间、缩短巴比妥钠睡眠潜伏期（P〈0．05或P〈0．01）和增加入睡动物发生率；灵芝提取物能显著增强小鼠迟发性变态反应、碳廓清能力和免疫脏器指数（P〈0．05）；复合制剂能显著增强小鼠迟发性变态反应（P〈0．05），对小鼠碳廓清能力和免疫脏器指数无显著影响。结论：灵芝提取物及复合制剂对小鼠睡眠和免疫功能有一定的改善作用。     

红菇提取液抗运动性疲劳作用的研究

目的：探讨红菇抗运动性疲劳的功效。方法：以容县红菇子实体为材料,昆明小鼠为试验对象,采用不同剂量的红菇子实体提取液对试验组小鼠连续灌胃21d后,对试验组与对照组的小鼠游泳力竭时间、乳酸脱氢酶、肝糖原含量等指标进行检测,研究容县野生红菇子实体提取液抗运动性疲劳作用。结果：经21d连续灌胃红菇子实体提取液的小鼠负重游泳时间与对照组相比显著延长;肝糖原含量比对照组显著提高,乳酸脱氢酶活力比对照组显著降低。结论：红菇提取液均能增强机体对运动负荷的适应能力、抵抗疲劳的产生和加速疲劳的消除,具有一定的抗疲劳作用。     

灵芝发酵茶提取液对小鼠抗疲劳作用的研究

试验采用BABL/c小鼠，按体重随机分为对照组和灵芝发酵茶高（4.198g/kg）、中(3.358g/kg）、低（2.798g/kg）剂量组。连续给样30d，末次给样30min后，进行小鼠负重游泳试验与测定血清尿素氮、血乳酸和肝糖原三个生化指标的抗疲劳试验。结果表明，一定剂量的灵芝发酵茶提取液有显著的抗疲劳作用。     

羊肚菌水提物对急性肝损伤的干预作用

研究羊肚菌水提物对CCl4致小鼠急性肝损伤的保护作用。预防给药16d后．采用CCl4复制小鼠急性肝损伤模型，24h后。眼眶取血．测定血清中丙氨酸氨基转移酶（ALT）、超氧化物歧化酶（SOD）、丙二醛（MDA）以及血清蛋白的变化．观察羊肚菌水提物对急性肝损伤的保护作用。羊肚菌水提物能明显降低模型组的血清转氨酶、肝脂质过氧化物含量抑制蛋白流失及肝脏肿大．说明羊肚菌水提物对小鼠肝脏的化学损伤有显著的保护作用．     

Effect of curcumin on scopolamine-induced memory impairment in mice

AIM:Scopolamine blocks cholinergic transmission and impairs learning and memory in mice. The purpose of this study was to evaluate the memory-improving properties of curcumin on scopolamine-induced memory impairment in mice. METHODS:The mice of memory impairment were induced by scopolamine. Step down test and Morris water maze test were used to observe the learning and memory ability in curcumin-treated mice. Biochemical assessments of AChE, MDA, and GSH-Px levels in brains were performed. RESULTS:Oral administration of curcumin significantly reduced the numbers of step-down errors (P<0.05) and prolonged the step-down latency induced by scopolamine (P<0.05). The escape latency time in mice treated with curcumin was remarkably reduced compared to that in scopolamine group by Morris water maze test (P<0.05). After the platform was removed, the total time that the mice swam in the target quadrant was also longer in curcumin group than that in model group (P<0.05). The data also indicated that curcumin significantly inhibited AChE activity (P<0.01) and prevented oxidative stress characterized by the significant reduction in MDA content and the significant increase in GSH-Px activities in the brain (P<0.01). CONCLUSION:Curcumin induces cognitive improvement by enhancing the function of cholinergic system and its antioxidant activity.     

Effects of rolipram on learning and memory and the activity of PDE4 in hippocampus following the focal brain injury induced by ischemia- reperfusion in rats

AIM: To investigate the effects of rolipram on the ability of learning and memory and the activity of PDE4 in hippocampus following the focal brain injury induced by ischemia- reperfusion in rats. METHODS: The cerebral ischemia-reperfusion injury model was made by middle cerebral artery occlusion (MCAO) in rats. The rats were randomly divided into sham-operated group, model group, and rolipram group. Rolipram was administered once a day (1 mg/kg, ip) from 6 h after the onset of the operation for 2 weeks. Then the learning and memory abilities were tested after Morris water maze and step-though training. The activity of PDE4 in hippocampus was evaluated by HPLC. RESULTS: In the Morris water maze test, compared to sham-operated group, the platform-finding time and swimming distance in model group were significantly longer (P<0.05). Compared to model group, the platform-finding time and swimming distance in rolipram group were significantly shorter (P<0.05). In the step-through test, compared to sham-operated group, the lantent period in model group was significantly shorter (P<0.01) and the error times were statistically increased(P<0.05). Compared with model group, the lantent period in rolipram group were significantly longer (P<0.05), and the error times were markedly decreased. The assay of the HPLC demonstrated that the activities of PDE4 in hippocampus in model group were higher than those in the sham-operated group and rolipram group. CONCLUSION: Rolipram reduces the activity of PDE4 in hippocampus and enhances the ability of learning and memory after the injury induced by ischemia-reperfusion.     

A dopamine receptor antagonist modulates or enhances the analgesia of morphine and analysis of their synergetic analgesic mechanism

AIM:To observe the synergetic analgesic effects of low dose of haloperidol, a dopamine antagonist and under-threshold dose of morphine on mice induced by thermal and acetic acid, and to analyze the major mechanism of their synergetic actions. METHODS:To examine the analgesic synergetic effect of haloperidol (0.315 mg/kg, 0.625 mg/kg, 1.25 mg/kg, ip respectively), morphine (3.125 mg/kg, 6.25 mg/kg, 12.5 mg/kg ip, respectively) or combining effect of haloperidol (0.3125 mg/kg) with morphine (3.125 mg/kg) on mice, we compared the change of pain threshold stimulated by thermal, latent period of twisting, the number of times of twisting by acetic acid, and we also estimated the antagonistic effect of d-amphetamine (10 mg/kg) and naloxone (5 mg/kg) on haloperidol and morphine group. RESULTS:Combination of haloperidol with morphine significantly enhanced pain threshold of mice induced by thermal,prolonged latent period of twisting and decreased the number of times of twisting.Naloxone markedly antagonized the combination of analgesic action of haloperidol and morphine and not d-amphetamine.CONCLUSION:Combination of haloperidol with morphine have synergetic analgesic effect and morphine is the dominant factor.     

金顶侧耳菌丝体提取物的动物免疫增强功能初探

本文研究了金顶侧耳对小白鼠腹腔巨噬细胞吞噬功能的作用 ,结果表明 :分别以 2 0mg/kg d、 10 0mg/kg d、剂量的金顶侧耳水提物对小白鼠进行腹腔注射 ,可明显提高小白鼠腹腔巨噬细胞的吞噬能力 ,与对照相比 ,效果极显著 ;但 10mg/kg d的剂量未能引起腹腔巨噬细胞吞噬能力的显著提高     

Effects of taurine-zinc on learning and memory abilities of vascular dementia mice

AIM:To observe the effects of taurine-zinc (TZC) on the learning and memory abilities of vascular dementia (VD) mice and to investigate the related mechanism. METHODS:The mice were randomly divided into model group, sham group, and TZC at 50 mg/kg, 100 mg/kg and 200 mg/kg groups. The mice in drug groups were given TZC by gavage at 10 mL/kg once daily. The mice in sham group and model group were given equal volume of distilled water. VD mice were established by intercepting both common carotid arteries and bleeding at caudal vein after 14 d of gavage. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by ELISA. The levels of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) were measured via spectrophotometer. Step-down test and Morris water maze test were used to examine the abilities of learning and memory in the mice. RESULTS:TZC at 50 mg/kg, 100 mg/kg and 200 mg/kg reduced the levels of TNF-α, IL-1β, iNOS and NO in the brain tissues. In the water maze test, TZC at 100 mg/kg and 200 mg/kg significantly decreased the error times and latency compared with model group. In the step-down test, the escape latency was prolonged and error times were lowered significantly by treatment with TZC at 50 mg/kg, 100 mg/kg and 200 mg/kg as compared with model group. CONCLUSION:TZC improves the abilities of learning and memory, which might be related to the reduction of TNF-α, IL-1β, iNOS and NO levels in VD mice.     

Effects of melatonin on gut motility

AIM: To investigate the influence of melatonin at different concentrations on the gut motility. METHODS: Male C57BL mice were used in the study. The mice were intraperitoneally injected with melatonin at doses of 1 mg/kg, 5 mg/kg, 50 mg/kg and 75 mg/kg. The colon bead expulsive time was measured at 15 min and 45 min after injection. The melatonin antagonist luzindole at a dose of 5 mg/kg was used before injection of 75mg/kg melatonin. The gut transit time was also recorded with oral Evens blue after injection of melatonin. RESULTS: Compared with control group, melatonin at the dose of 1 mg/kg at 15 min decreased the colon bead expulsive time. However, melatonin at high dose (75 mg/kg) prolonged the colon bead expulsive time compared with the control, which was effectively blocked by melatonin antagonist luzindole. Compared with control group, injection of melatonin at the dose of 5 mg/kg at 45 min decreased the colon bead expulsive time. However, melatonin at high dose (75 mg/kg) prolonged the colon bead expulsive time. No difference of colon bead expulsive time between using 1 mg/kg and 50 mg/kg melatonin was observed. In whole gut transit time test, after injection of melatonin at the doses of 1 mg/kg and 5 mg/kg, the time was decreased. The expulsive time of fecal pellet with Evens blue was shorten as compared with control group. However, the gut transit time was significantly prolonged after high dose of melatonin (75 mg/kg) was used. CONCLUSION: Low dose of melatonin increases while high dose decreases the gut motility. Melatonin antagonist luzindole effectively blocks the latter effect.     

Effect of chronic intermittent hypoxia on memory and CREB expression in growing rats

AIM: To observe the alterations in cognition of growing rats exposed to chronic intermittent hypoxia (CIH) and to explore its underlying mechanisms. METHODS: Forty male Sprague-Dawley rats (3-week-old～4-week-old and 80 g to 100 g), which had been trained to complete the 8-arm (4-arm baited) radial maze, were randomly divided into 4 groups: 2-weeek-CIH group (2IH), 4-week-CIH group (4IH), 2-week-control group (2C) and 4-weeek-control group (4C). The intermittent hypoxia model was induced by putting the animals in an intermittent hypoxia cabin. When intermittent hypoxia was terminated, spatial memory of these growing rats was tested by 8-arm (4-arm baited) radial maze task, then, one rat in each group was randomly selected for ultrastructural observation. The hippocampus and prefrontal cortexes of the rats were collected for analyzing the mRNA and protein expression of CREB by RT-PCR and Western blotting, respectively. RESULTS: (1) In the 8-arm (4-arm baited) radial maze task, the results indicated that the rats in the 4 groups displayed significant difference in their performance assessed by three measuremens: the reference memory error, the working memory error and total memory error (P<0.05, respectively). (2) Early apoptosis and destructure of the neurons in the hippocampus and prefrontal cortex were observed under electron microscope in CIH exposed groups, especially in 4IH group, but not detected in 2C and 4C groups. (3) The expression levels of CREB mRNA and p-CREB protein in 2IH and 4IH groups were less than those in 2C and 4C groups in the hippocampus and prefrontal cortex (P<0.05, respectively), especially in the hippocampus of 4IH group (P<0.01). No difference was found within control groups (P>0.05, respectively). CONCLUSION: Exposure to experimentally-induced IH in growing rats is associated with time related spatial memory impairment. Chronic intermittent hypoxia leads to the disorders of neuron ultra-structure in memory related brain regions. It also inhabits the CREB transduction, expression and CREB phosphorylation, decreases the synthesis of the memory related protein. These factors maybe contribute to learning-memory impairment of growing rats exposed to chronic intermittent hypoxia.     

Effects of N-acetylcysteine on the lipopolysaccharide-induced MAPK phosphorylation in mouse liver

AIM: To investigate the effects of antioxidant N-acetylcysteine (NAC) on the lipopolysaccharide (LPS)-induced MAPK phosphorylation in mouse liver. METHODS: 54 male mice were divided into three groups: control (n=6), 0.9% sodium chloride 0.2 mL ip; LPS group (n=24): LPS 5 mg ip; NAC+LPS group (n=24): NAC 150 mg·kg-1·d-1 ip, for 3 d; LPS 5 mg ip after 1 h of NAC administration at 3rd day. The liver was excised with carbrital anesthesia after LPS or 0.9 % sodium chloride injection at 0.5 h, 1 h, 2 h and 6 h for GSH and MDA assays. The protein extracted from liver was assayed for the phosphorylation of MEK1/2, ERK1/2, p38 MAPK by Western blotting. TNF-α in liver was assayed by radioimmunoassay. RESULTS: MDA in the liver was decreased remarkably and the GSH in the liver was increased significantly by NAC pretreatment. The phosphorylation of MEK1/2, ERK1/2 and p38 MAPK in liver were inhibited significantly by NAC pretreatment after LPS challenge. Meanwhile, TNF-α in liver was decreased markedly. CONCLUSION: Reactive oxygen species plays a critical role in MAPK signaling during the LPS induced acute liver injury. NAC partially inhibits LPS-induced MAPK signaling by antioxidant effect and decreases TNF-α production.     

Effect of berberine and yohimbine on impaired enterocyte proliferation and intestinal injury in LPS-challenged mice

AIM: To evaluate the effects of oral berberine (Ber) and yohimbine (Y) in preventing intestinal damage and impaired enterocyte proliferation caused by lipopolysaccharide (LPS) in mice. METHODS: Male BALB/c mice were randomly divided into 8 groups: control, LPS, Ber+LPS, Ber+Y+LPS, Y+LPS, Ber, Ber+Y and Y. The mice were administered intragastrically with distilled water (0.1 mL/10 g), Ber (50 mg/kg), Ber (50 mg/kg) in combination with Y (2 mg/kg) or Y (2 mg/kg) once a day for 3 days. One hour after intragastrical treatment on the third day, LPS (18 mg/kg) or normal saline was injected intraperitoneally. Twenty hours after LPS administration, the histological changes of the intestine were observed, and injury score was assessed. The mucosal weight, villus height and the content of diamine oxidase (DAO) in the ileum were also measured. Furthermore, the proliferation of enterocyte was identified by immunohistochemical staining for proliferating cell nuclear antigen (PCNA). RESULTS: Compared to the control mice, the mice challenged with LPS resulted in intestinal injury, including significantly increased injury score, decreased gut mucosa weight, villus height and the DAO contents in ileum. Furthermore, enterocyte proliferation was inhibited significantly 12 h after LPS challenge. Pretreatment with Ber or Ber+Y significantly inhibited the intestinal injury, and attenuated the impairment of enterocyte proliferation induced by LPS. However, no significant difference in the above parameters between Ber+LPS group and Ber+Y+LPS group was observed. Treatment with Y only did not prevent LPS-induced intestinal injury. CONCLUSION: Pretreatment with berberine remarkably reduces LPS-induced intestinal injury and the impairment of enterocyte proliferation in an alpha 2 adrenoceptor-independent manner.