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目的观察H2O2诱导原代培养SD大鼠视网膜细胞凋亡过程中细胞内Ca2＋浓度（[Ca2＋]i）的变化及其来源。方法取1-3d内新生SD大鼠视网膜进行原代细胞培养,以100μmol/L H2O2作用0、2、4、8、12、24h,采用MTT法进行细胞活力检测,应用Hoechst 33342染色法进行细胞凋亡检测,以Fluo-3AM为细胞内Ca2＋探针并利用荧光激活细胞分类技术（FACS）进行[Ca2＋]i检测,确定H2O2诱导细胞损伤及凋亡过程中[Ca2＋]i的变化;应用细胞外Ca2＋螯合剂EGTA初步检测H2O2诱导的[Ca2＋]i变化是否源于细胞外Ca2＋内流。结果 100μmol/L H2O2可诱导原代培养的SD大鼠视网膜细胞发生凋亡,且凋亡数目呈时间依赖性递增;100μmol/L H2O2作用2-24h均可显著降低细胞活力,而[Ca2＋]i的升高出现在H2O2作用2h且维持至12h,然后逐渐下降,至24h恢复至正常水平;0.5-5mmol/L EGTA可显著削弱由100μmol/L H2O2作用2h导致的[Ca2＋]i增加。结论在H2O2诱导原代培养的SD大鼠视网膜细胞发生凋亡过程中,[Ca2＋]i的升高发生在凋亡的早期阶段,而非细胞凋亡全过程中;H2O2的损伤作用所导致的[Ca2＋]i升高部分来源于细胞外Ca2＋的内流。

目的探讨高脂饮食对大鼠甜味觉敏感性的影响。方法刚断乳雄性SD大鼠，适应1周后，高脂饮食喂养2周，按体质量增加程度将实验动物分为3组，即肥胖易感组（obesityprone，OP）、肥胖抵抗（obesityresistant，0R）组和对照组（control，C）。OP及OR组继续喂养高脂饲料，对照组转由正常饲料喂养（c—C），连续8周。采用条件性厌味（CTA）及双瓶选择实验，检测大鼠对甜味的喜好及其阈值变化，并测定大鼠热量总摄入量和食物转化效率。结果①高脂喂养的OP大鼠体质量增加明显高于0R及对照组大鼠，而对照组大鼠体质量增加又高于高脂喂养的OR大鼠。②高脂喂养的大鼠（OP与OR）的蔗糖阈值明显低于正常对照组大鼠，但OP与OR大鼠之间的蔗糖阈值无差异。③高脂喂养大鼠（OP与0R）的蔗糖喜好明显高于正常对照组大鼠，而OP与OR大鼠之间的蔗糖喜好无差异。④高脂喂养的0P大鼠总热量摄入明显高于OR大鼠，但高脂饲料喂养与正常饲料喂养的大鼠总热量摄入无差异。⑤高脂喂养的OP大鼠食物效率明显高于OR大鼠及正常对照大鼠，而高脂喂养的OR大鼠食物效率与正常对照大鼠无差异。结论高脂饮食可通过增高大鼠甜味敏感性，从而影响摄食行为并引起肥胖。

目的比较SD、E3与DA1U大鼠视网膜光损伤敏感性,为构建不同品系大鼠视网膜光损伤模型和研究眼底色素抗光损伤保护视网膜的相关机制研究提供实验依据。方法成年SD、E3、DA1U大鼠,雌雄随机选取,采用视网膜电图与HE染色分别检测正常情况下与光损伤后不同品系大鼠视网膜感光功能与组织形态变化,采用TUNEL染色观察光损伤后视网膜凋亡细胞的分布与数量。结果正常状态下,SD大鼠色素上皮层、脉络膜层及E3大鼠色素上皮层均无色素分布,而E3大鼠脉络膜层、DA1U大鼠色素上皮层与脉络膜层有褐色色素分布;HE结果显示,在正常状态下,3种品系大鼠视网膜外核层厚度没有显著差异,而在光损伤条件下,SD大鼠视网膜各层细胞均严重受损;视网膜电图结果显示,在正常状态下,不同品系大鼠间视网膜电图视杆细胞反应b波振幅存在显著差异,E3大鼠最大混合反应a波及b波振幅与SD大鼠相比有显著差异,而在光损伤条件下,与SD大鼠相比,E3和DA1U大鼠视网膜电图a波与b波的波幅降幅显著减弱;TUNEL染色结果显示,与SD大鼠相比,E3与DA1U大鼠视网膜内核层及外核层凋亡细胞分布范围与数量均显著下降。结论 SD、E3与DA1U大鼠间存在视网膜色素分布与光...

细胞内钙超载在急性胰腺炎中发挥关键性作用，而白藜芦醇可以减轻胰腺炎的严重程度。有关白藜芦醇治疗胰腺炎的机制尚未明确。本研究旨在阐明细胞内钙离子调节失衡和白藜芦醇对大鼠急性胰腺炎的治疗效应间的关系。将雄性SD大鼠随机分成3组：假手术组（OS）、重症急性胰腺炎组（SAP）和白藜芦醇治疗组（RES）。通过胰胆管逆行注射牛磺胆酸钠建立重症急性胰腺炎模型，而白藜芦醇通过静脉给药。

Aim： Microvesicles （MVs） are nanoscale membrane fragments released from virtually all cell types upon activation or apoptosis, and may contribute to the beneficial effects of stem cell therapy. In this study, we investigated the therapeutic effects of mesenchymal stem cell （MSC） derived MVs （MSC-MVs） on pulmonary artery hypertension （PAH） in rats. Methods： MSC-MVs were isolated from rat bone marrow MSCs that were cultured in a serum-free conditioned medium. Transmission electron microscopy （TEM）, flow cytometry and nanoparticle tracking analysis （NTA） were used to characterize the MVs. Adult SD rats were injected with monocrotaline （50 mg/kg, sc） to induce PAH. Three weeks later, the rats were intravenously injected with MSCs, MSC-MVs or saline for 2 weeks. At the end of treatments, the hemodynamic parameters and pathological right ventricular and pulmonary arterial remodeling were analyzed in each group. Results： The MSC-MVs showed general morphologic characteristics of MVs and expressed annexin V and CD29 markers under TEM, and their size ranged from 40 to 300 nm. Intravenous injection of MSC-MVs or MSCs significantly ameliorated the mean pulmonary artery pressure （mPAP） and mean right ventricle pressure （mRVP） in PAH rats. Furthermore, intravenous injection of MSC-MVs or MSCs significantly decreased the right ventricle （RV） hypertrophy and pulmonary arteriole area index （AI） and thickness index （TI） in PAH rats. Conclusion： Intravenous injection of MSC-MVs or MSCs produces similar beneficial effects for treating PAH, and our results provide a basis for cell-free approach in stem cell therapy.

Evidence suggests that the hyperammonemia （HA）-induced neuroinflammation and alterations in the serotonin （5-HT） system may contribute to cognitive decline and anxiety disorder during hepatic encephalopathy （HE）. Probiotics that maintain immune system homeostasis and regulate the 5-HT system may be potential treatment for HA-mediated neurological disorders in HE. In this study, we tested the efficacy of probiotic Lactobacillus helveticus strain NS8 in preventing cognitive decline and anxie- ty-like behavior in HA rats. Chronic HA was induced by intraperitoneal injection of ammonium acetate for four weeks in male Sprague-Dawley rats. HA rats were then given Lactobacillus helveticus strain NS8 （109 CFU mL 1） in drinking water as a dai- ly supplementation. The Morris water maze task assessed cognitive function, and the elevated plus maze test evaluated anxie- ty-like behavior. Neuroinflammation was assessed by measuring the inflammatory markers： inducible nitric oxide synthase, prostaglandin E2, and interleukin-1 13 in the brain. 5-HT system activity was evaluated by measuring 5-HT and its metabolite, 5-HIAA, and the 5-HT precursor, tryptophan. Probiotic treatment of HA rats significantly reduced the level of inflammatory markers, decreased 5-HT metabolism, restored cognitive function and improved anxiety-like behavior. These results indicate that probiotic L. helveticus strain NS8 is beneficial for the treatment of cognitive decline and anxiety-like behavior in HA rats.

Chronic periodontitis （CP） is one of the most common oral diseases, which causes alveolar bone absorption and tooth loss in adults. in this study we aimed to investigate the potential of plumbagin （PL）, a widely-investigated active compound extracted from the traditional Chinese herb Plumbago zeylanica L in treating CP. Human periodontal ligament stem cells （PDLSCs） were used for in vitro studies, whereas an animal model of CP was established in SD rats by ligation＋Porphyromonas gingivalis （Pg） stimulation. The rats were injected with PL （2, 4, and 6 mg·kg^-1·d^-1, ip） for 4 weeks. Treatment of PDLSCs with TNF-α （10 ng/mL） markedly stimulated the expression of the proinflammatory cytokines TNF-α, IL-1β and IL-6, as well as the chemokines CCL-2 and CCL-5, which were dose- dependently suppressed by co-treatment with PL （1.25-5 μmol/L）. Furthermore, PL （3.75 pmol/L） markedly suppressed TNF-α-induced activation of the MAPK, NF-κB and JAK/STAT signaling pathways in PDLSCs. In consistence with the in vitro studies, PL administration significantly decreased the expression of TNF-α, IL-1β and IL-6 in gingiva of the rat with CP, with the dosage 4 mg·kg^-1·d^-1 showing the best anti-inflammatory effect. Moreover, PL administration decelerated bone destruction in the rat with CP, evidenced by the aveolar bone loss （ABL） and H＆E staining results. In conclusion, PL suppresses CP progression in rats by downregulating the expressions of TNF-α, IL-1β and IL-6 and inhibiting the MAPK, NF-κB and JAK/STAT signaling pathways.

Aim： Homocysteine （Hcy） can elicit neuronal cell death, and hyperhomocysteinemia is a strong independent risk factor for Alzheimer’s disease. The aim of this study was to examine the effects of hydrogen sulfide （H2S） on Hcy-induced endoplasmic reticulum （ER） stress and neuronal apoptosis in rat hippocampus. Methods： Adult male SD rats were intracerebroventricularly （icv） injected with Hcy （0.6 μmol/d） for 7 d. Before Hcy injection, the rats were treated with NaHS （30 or 100 μmol·kg^-1·d^-1, ip） and/or k252a （1 μg/d, icv） for 2 d. The apoptotic neurons were detected in hippocampal coronal slices with TUNEL staining. The expression of glucose regulated protein 78 （GRP78）, C/EBP homologous protein （CHOP）, cleaved caspase-12, and BDNF in the hippocampus were examined using Western blotting assays. The generation of H2S in the hippocampus was measured with the NNDPD method. Results： Hcy markedly inhibited the production of endogenous H2S and increased apoptotic neurons in the hippocampus. Further-more, Hcy induced ER stress responses in the hippocampus, as indicated by the upregulation of GRP78, CHOP, and cleaved caspase-12. Treatment with the H2S donor NaHS increased the endogenous H2S production and BDNF expression in a dose-dependent manner, and significantly reduced Hcy-induced neuronal apoptosis and ER stress responses in the hippocampus. Treatment with k252a, a specific inhibitor of TrkB （the receptor of BDNF）, abolished the protective effects of NaHS against Hcy-induced ER stress in the hippocampus. Conclusion： H2S attenuates ER stress and neuronal apoptosis in the hippocampus of Hcy-treated rats via upregulating the BDNF-TrkB pathway.

Aim： Arctigenin, a phenylpropanoid dibenzylbutyrolactone lignan found in traditional Chinese herbs, has been determined to exhibit a variety of pharmacological activities, including anti-tumor, anti-inflammation, neuroprotection, and endurance enhancement. In the present study, we investigated the antioxidation and anti-fatigue effects of arctigenin in rats. Methods： Rat L6 skeletal muscle cell line was exposed to H202 （700 pmol/L）, and ROS level was assayed using DCFH-DA as a probe. Male SD rats were injected with arctigenin （15 mg.kg-1., ip） for 6 weeks, and then the weight-loaded forced swimming test （WFST） was performed to evaluate their endurance. The levels of antioxidant-related genes in L6 cells and the skeletal muscles of rats were analyzed using real-time RT-PCR and Western blotting. Results： Incubation of L6 cells with arctigenin （1, 5, and 20 pmol/L） dose-dependently decreased the H2O2-induced ROS production. WFST results demonstrated that chronic administration of arctigenin significantly enhanced the endurance of rats. Furthermore, molecular biology studies on L6 cells and skeletal muscles of the rats showed that arctigenin effectively increased the expression of the antioxidant-related genes, including superoxide dismutase （SOD）, glutathione reductase （Gsr）, glutathione peroxidase （GPX1）, thioredoxin （Txn） and uncoupling protein 2 （UCP2）, through regulation of two potential antioxidant pathways： AMPK/PGC-1α/PPARα in mitochondria and AMPK/p53/Nrf2 in the cell nucleus. Conclusion： Arctigenin efficiently enhances rat swimming endurance by elevation of the antioxidant capacity of the skeletal muscles, which has thereby highlighted the potential of this natural product as an antioxidant in the treatment of fatigue and related diseases.

Aim： To investigate whether strontium ranelate （SR）, a new antiosteoporotic agent, could attenuate cartilage degeneration and sub- chondral bone remodeling in osteoarthritis （OA）. Methods： Medial meniscal tear （MMT） operation was performed in adult SD rats to induce OA. SR （625 or 1800 mg·kg^-1·d^-1） was administered via gavage for 3 or 6 weeks. After the animals were sacrificed, articular cartilage degeneration was evaluated using toluidine blue 0 staining, SOX9 immunohistochemistry and TUNEL assay. The changes in microarchitecture indices and tissue mineral density （TMD）, chemical composition （mineral-to-collagen ratio）, and intrinsic mechanical properties of the subchondral bones were measured using micro-CT scanning, confocal Raman microspectroscopy and nanoindentation testing, respectively. Results： The high-dose SR significantly attenuated cartilage matrix and chondrocyte loss at 6 weeks, and decreased chondrocyte apop- tosis, improved the expression of SOX9, a critical transcription factor responsible for the expression of anabolic genes type II collagen and aggrecan, at both 3 and 6 weeks. Meanwhile, the high-dose SR also significantly attenuated the subchondral bone remodeling at both 3 and 6 weeks, as shown by the improved microarchitecture indices, TMD, mineral-to-collagen ratio and intrinsic mechanical prop- erties. In contrast, the low-dose SR did not significantly change all the detection indices of cartilage and bone at both 3 and 6 weeks. Conclusion： The high-dose SR treatment can reduce articular cartilage degeneration and subchondral bone remodeling in the rat MMT model of OA.