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排序方式: 共有1754条查询结果,搜索用时 31 毫秒
1.
目的探讨神经妥乐平对帕金森病(PD)大鼠的神经保护作用及其相关机制。方法 SD大鼠分为对照组、PD组(PD造模)、神经妥乐平低剂量组(PD造模+腹腔注射0.6 Nu·kg-1神经妥乐平溶液)、神经妥乐平高剂量组(PD造模+腹腔注射1.2 Nu·kg-1神经妥乐平溶液)和通路抑制组(PD造模+腹腔注射1.2 Nu·kg-1神经妥乐平溶液及2 mg·k-1 Nrf2通路抑制剂Brusatol)。转棒试验及爬杆试验测试大鼠的行为功能,记录跌落潜伏期、爬下时间;苏木精-伊红染色观察脑组织病理变化;试剂盒检测脑组织中过氧化氢酶(CAT)活性、丙二醛(MDA)含量及白细胞介素(IL)-6、IL-1β水平;蛋白印迹检测脑组织中核因子E2相关因子2 (Nrf2)、血红素加氧酶-1 (HO-1)和醌氧化还原酶1 (NQO1)蛋白表达。结果与对照组相比,PD组大鼠跌落潜伏期显著缩短(P<0.05),脑组织中CAT活性、Nrf2、HO-1、NQO1蛋白表达水平显著降低(P<0.05),爬下时间显著延长(P<0.05),脑组织中MDA含量、IL-6、IL-1 β水平显著升高(P<0.05),脑组织出现病理改变;与PD组相比,神经妥乐平低、高剂量组大鼠跌落潜伏期显著延长(P<0.05),脑组织中CAT活性、Nrf2、HO-1、NQO1蛋白表达水平显著升高(P<0.05),爬下时间显著缩短(P<0.05),脑组织中MDA含量、IL-6、IL-1 β水平显著降低(P<0.05),脑组织病变减轻;与神经妥乐平高剂量组相比,通路抑制组大鼠跌落潜伏期显著缩短(P<0.05),脑组织中CAT活性、Nrf2、HO-1、NQO1蛋白表达水平显著降低(P <0.05),爬下时间显著延长(P <0.05),脑组织中MDA含量、IL-6、IL-1 β水平显著升高(P<0.05),脑组织病变程度加重。结论神经妥乐平可改善脑组织氧化应激、炎症损伤状态,提高PD大鼠行为功能,其机制可能与激活Nrf2/HO-1/NQO1通路有关。  相似文献   
2.
《Saudi Pharmaceutical Journal》2022,30(11):1561-1571
ObjectivesHuangpu Tongqiao Capsule (HPTQC) is a traditional Chinese medicine (TCM) that has been used to treat Alzheimer's disease (AD). This study was to explore the pharmacological action and molecular mechanism of HPTQC in the treatment of AD.MethodsThe possible targets of HTPQC were predicted by the molecular docking technique. Intraperitoneal injection of D-galactose and bilateral injection of Aβ25-35 in hippocampus induced AD rat model. Morris water maze was used to observe learning and memory function. The primary hippocampal neurons were induced by Aβ25-35. Moreover, the apoptosis rate of hippocampal nerve cells was detected through AnnexinV/PI double standard staining. The mRNA and protein levels of GRP78, CHOP, Caspase 12, Caspase 9, and Caspase 3 were detected by PCR and western blot.ResultsThe prediction results suggest that HPTQC may act on GRP78. HPTQC significantly improved the learning and memory function, and decreased neuronal apoptosis in vivo and in vitro. In addition, HPTQC could decrease the mRNA and protein expression levels of GRP78, CHOP, Caspase12, Caspase9, and Caspase3, and the effect trend was consistent with the specific inhibitor of GRP78.ConclusionsHPTQC has a neuroprotective effect against AD by inhibiting the apoptosis pathway mediated by endoplasmic reticulum stress.  相似文献   
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肛提肌外腹会阴联合切除术(ELAPE)已经成为治疗低位进展期直肠癌的重要术式。在降低局部复发率的同时,ELAPE手术由于切除更多肿瘤周围组织,有可能增加泌尿生殖神经损伤的发生率。笔者认为,在ELAPE手术的会阴操作过程中,对盆丛、阴部神经和神经血管束的保护是可行的,有助于保留术后的泌尿功能和性功能。在术前MRI分期的指导下,结合肿瘤的垂直浸润深度和环周生长情况,提出的个体化ELAPE技术,有助于在保证肿瘤根治性前提下,进一步减少手术创伤和保护会阴部神经。  相似文献   
5.
Bisphenol A (BPA), a well-recognized anthropogenic xenoestrogen, has been identified as a causative agent responsible for inducing carcinogenicity, cognitive impairment, neurotoxicity, oxidative stress, etc. However, BPA-induced neurotoxicity and its possible amelioration through natural compound intervention remain elusive. The current study was performed to elucidate the neurotoxic potential of BPA in zebrafish (Danio rerio) by waterborne exposure and its possible amelioration by quercetin co-supplementation. Protective effect of quercetin against BPA-induced altered neurobehavioral response, oxidative stress and neuromorphological changes were evaluated in zebrafish brain. The present findings reveal that BPA-induced altered neurobehavioral response was ameliorated by quercetin. Biochemical studies advocate the potential therapeutic efficacy of quercetin against BPA-induced oxidative stress in zebrafish brain. Quercetin also shows neuroprotection against BPA-induced augmented neuronal pyknosis in periventricular grey zone (PGZ) of zebrafish brain. These basic findings indicate that quercetin may act as an effective intervention against BPA-induced neurotoxicity in zebrafish through down-regulation of oxidative stress.  相似文献   
6.
Menopause involves dramatic declines in estradiol production and levels. Importantly, estradiol and the class of stress hormones known as glucocorticoids exert countervailing effects throughout the body, with estradiol exerting positive effects on the brain and cognition, glucocorticoids exerting negative effects on the brain and cognition, and estradiol able to mitigate negative effects of glucocorticoids. Although the effects of these hormones in isolation have been extensively studied, the effects of estradiol on the stress response and the neuroprotection offered against glucocorticoid exposure in humans are less well known. Here we review evidence suggesting that estradiol-related protection against glucocorticoids mitigates stress-induced interference with cognitive processes. Animal and human research indicates that estradiol-related mitigation of glucocorticoid damage and interference is one benefit of estradiol supplementation during peri-menopause or soon after menopause. The evidence for estradiol-related protection against glucocorticoids suggests that maintaining estradiol levels in post-menopausal women could protect them from stress-induced declines in neural and cognitive integrity.  相似文献   
7.
The potential ability of melatonin to protect against impairment of the fetal peripheral nerve system due to maternal consumption of diclofenac sodium (DS) was investigated. Eighty-four pregnant rats were divided into seven groups: control (CONT), saline administered (PS), DS administered (DS), DS with low-dose melatonin administered (DS + MLT10), DS with high-dose melatonin administered (DS + MLT50), low-dose melatonin administered (MLT10), and high-dose melatonin administered (MLT50). After the pregnancy, six male newborn rats from each group were sacrificed at 4 and 20 weeks of age. Their right sciatic nerves were harvested, and nerve fibers were evaluated using stereological techniques. Mean numbers of myelinated axons, axon cross-section areas and the mean thickness of the myelin sheet were estimated. Four-week-old prenatally DS-exposed rats had significantly fewer axons, a smaller myelinated axonal area, and a thinner myelin sheath compared to CONT group (p < 0.05). Although melatonin at both doses significantly increased axon numbers, only a high dose of melatonin increased the diameter of those axons (p < 0.05). At 20-weeks of age, myelinated axon number in the DS group was not only significantly lower than all other groups (p < 0.05) but also the cross-sectional area of these axons was smaller than all other groups (p < 0.05). There were no differences between the groups regarding the mean thickness of the myelin sheet. The current study indicates that prenatal exposure to DS decreases the number and the diameter of sciatic nerve axons and that melatonin prophylaxis can prevent these effects.  相似文献   
8.
The steroid hormone 17b-estradiol and the peptide hormone insulin-like growth factor (IGF)-1 independently exert neuroprotective actions in neurologic diseases such as stroke. Only a few studies have directly addressed the interaction between the two hormone systems, however, there is a large literature that indicates potentially greater interactions between the 17b-estradiol and IGF-1 systems. The present review focuses on key issues related to this interaction including IGF-1 and sex differences and common activation of second messenger systems. Using ischemic stroke as a case study, this review also focuses on independent and cooperative actions of estrogen and IGF-1 on neuroprotection, blood brain barrier integrity, angiogenesis, inflammation and post-stroke epilepsy. Finally, the review also focuses on the astrocyte, a key mediator of post stroke repair, as a local source of 17b-estradiol and IGF-1. This review thus highlights areas where significant new research is needed to clarify the interactions between these two neuroprotectants.  相似文献   
9.
Limited research has evaluated the corticosteroids (CS) response in hypoxic preconditioning (PC) induced neuroprotection against subsequent hypoxic-ischemic (HI) brain injury in newborns. To measure, CS response to hypoxic PC, at postnatal day 6 (P6), rat pups were randomly divided into sham, NoPC (exposure to 21% O2) and PC (exposure to 8% O2 for 3 h) groups. In a separate experiment, at P6, rat pups were randomly divided into three groups (sham, NoPC + HI, PC + HI). Rat pups in NoPC + HI and PC + HI groups, respectively had normoxic or hypoxic exposure for 3 h at P6 and then had the right carotid artery permanently ligated followed by 140 min of hypoxia at P7 (HI). Plasma CS levels were measured at 0.5, 1, 3, 6 and 12 h after hypoxic PC and hypoxic PC followed by HI. To investigate whether CS response to hypoxic PC provides neuroprotection against HI, at P6, rat pups were randomly divided into five groups. Fifteen minutes prior to PC or normoxic exposure, rat pups in DMSO + PC + HI and DMSO + NoPC + HI groups received DMSO while in RU486 + PC + HI and RU486 + NoPC + HI groups received RU486 (glucocorticoid receptor blocker, 60 mg/kg) s.c., respectively. Afterwards, rat pups were exposed to normoxia (DMSO + NoPC + HI, RU486 + NoPC + HI) or hypoxia (DMSO + PC + HI, RU486 + PC + HI) for 3 h and then HI 24 h later (P7). Rat pups at the corresponding age without any exposure to PC or HI or RU486/DMSO were used as sham. We found that hypoxic PC caused CS surge as well as augmented CS surge and preserved the glucocorticoid feedback regulation after HI. Hypoxic PC reduced HI induced early and delayed brain damage. RU486 partially but significantly inhibited hypoxic PC induced neuroprotection.  相似文献   
10.
目的基于磷酯酰激醇3-激酶/蛋白激酶B(PI3K/Akt)通路探讨氯吡格雷对脑缺血再灌注损伤大鼠的神经保护作用.方法建立脑缺血再灌注大鼠模型,随机分为模型组、氯吡格雷组、LY294002(PI3K抑制剂)组、氯吡格雷+LY294002组,每组12只,另取12只SD大鼠设为假手术组.分组处理后,所有大鼠进行神经功能缺损评分并尾静脉取血,处死大鼠,HE染色检测各组大鼠神经元病理情况;三苯基氯化四氮唑(TTC)染色检测各组大鼠脑组织梗死面积;ELISA检测血清中中枢神经特异性蛋白(S100β)、神经元特异性烯醇化酶(NSE)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平;蛋白免疫印迹法检测脑组织中PI3K/Akt通路蛋白表达情况.结果与假手术组相比,模型组大鼠脑组织神经元出现坏死、核收缩变小等病理变化,神经功能缺损评分、脑梗死面积、血清中S100β、NSE、IL-6及TNF-α水平均明显升高(P<0.05),脑组织中p-PI3K/PI3K、p-Akt/Akt明显降低(P<0.05);与模型组相比,氯吡格雷组大鼠神经元病理损伤减轻,神经功能缺损评分、脑梗死面积、血清中S100β、NSE、IL-6及TNF-α水平均降低(P<0.05),脑组织中p-PI3K/PI3K、p-Akt/Akt升高(P<0.05);LY294002组大鼠神经元病理损伤加重,神经功能缺损评分、脑梗死面积、血清中S100β、NSE、IL-6及TNF-α水平均升高(P<0.05),脑组织中p-PI3K/PI3K、p-Akt/Akt降低(P<0.05).与LY294002组相比,氯吡格雷+LY294002组大鼠神经元病理损伤减轻,神经功能缺损评分、脑梗死面积、血清中S100β、NSE、IL-6及TNF-α水平均降低(P<0.05),脑组织中p-PI3K/PI3K、p-Akt/Akt升高(P<0.05).与氯吡格雷组相比,氯吡格雷+LY294002组大鼠神经元病理损伤加重,神经功能缺损评分、脑梗死面积、血清中S100β、NSE、IL-6及TNF-α水平均升高(P<0.05),脑组织中p-PI3K/PI3K、p-Akt/Akt降低(P<0.05).结论氯吡格雷可通过激活PI3K/Akt通路减轻大鼠脑缺血再灌注损伤,保护脑组织.  相似文献   
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