铜钱树种子休眠特性及破眠技术研究

通过形态解剖、破损种皮以及激素处理等,探讨铜钱树种子休眠原因及破除休眠的方法。结果表明,铜钱树种子存在硬实现象,空瘪粒也较高。铜钱树果壳和种皮存在机械障碍,水分难以透过果壳,种皮表面存在蜡质层,对水分和空气有一定阻碍作用,未经赤霉素处理的种子较难萌发。铜钱树种子休眠主要由果壳、种皮限制以及生理休眠导致。赤霉素、过氧化氢浸泡1h和60℃热水处理在一定程度上均可破除种子休眠,促进萌发,但以100~150mg·L^-1赤霉素浸泡24h为打破种子休眠的最佳方法,且发芽率最高,为44.1%。     

茶树油粕中茶皂素的提取及其对果蔬采后致病菌的抑制作用

以从茶树油粕中提取茶皂素的得率为评价指标,研究提取溶剂、方法、时间、温度和料液比等因素对茶皂素得率的影响,并通过正交试验确定茶皂素最佳提取工艺条件,同时考察了所得茶皂素对几种果蔬采后致病菌的抑制作用。结果表明,茶树油粕中提取茶皂素的最佳工艺条件为:以75%乙醇作为提取溶剂,料液比1∶14(g/mL),85℃热回流提取2.5 h,茶皂素的得率达13.3%,经AB-8大孔吸附树脂纯化后,纯度达95.64%。所获茶皂素对胶胞炭疽菌(Colletotrichum gloeosporioides)、灰葡萄孢霉(Botrytis cinerea)和链格孢菌(Alternaria alternata)菌丝的生长均有显著的抑制作用,半最大效应浓度(EC50)值分别为203.62、165.87和550.61mg·L^-1,其中以对B. cinerea的抑制作用最强。     

药食同源莲子的应用研究进展

莲子营养价值丰富,既可药用又可食用,为"药食同源"产品之一。自古以来,莲子都是人们喜爱的滋补品,不仅补益效果佳、来源方便,还可以根据不同的搭配制作出多种类型的莲子保健产品。随着研究的深入,莲子的应用范围日益广泛,已渗透到中医药、保健食品开发、日化用品研发中,且市场开发前景巨大。     

花前施用6-BA对抗寒无核葡萄胚挽救效果的影响

在花前14 d,分别对4个抗寒无核葡萄杂交组合‘火焰无核’×00-1-5、‘秦红10号’×00-1-5、‘秦红2号’ב木星’和‘红宝石无核’×00-1-5的母本花序施用不同浓度6-BA,以MM3固液双相培养基作为胚发育培养基,WPM固体培养基作为胚萌发培养基进行胚挽救,研究花前施用6-BA对胚挽救效果的影响。结果表明:花前施用6-BA对胚的发育起促进作用,但不同浓度6-BA对不同杂交组合的胚挽救效果不同,其中‘秦红10号’×00-1-5、‘秦红2号’ב木星’和‘红宝石无核’×00-1-5在6-BA浓度为50mg/L时,胚发育率、萌发率和成苗率最高;而‘火焰无核’×00-1-5在6-BA浓度为30 mg/L时,胚发育率、萌发率和成苗率最高。无核品种‘秦红2号’‘红宝石无核’最适宜作母本,‘火焰无核’胚挽救效果较差。     

一株高致病力赭绿青霉的生物学特性及杀虫活性

为明确一株高致病力赭绿青霉Penicillium ochrochloron Q-1的生防潜力,室内测试了不同营养、环境因素及常见杀菌剂、杀虫剂对菌株Q-1的影响,并采用室内毒力测定方法研究菌株Q-1对不同昆虫的毒力。结果表明：菌株Q-1对营养要求较低,最适生长和产孢培养基分别为淀粉琼脂培养基（SYA）和马铃薯葡萄糖琼脂培养基（PDA）,最适生长碳源为麦芽糖,最适产孢碳源为葡萄糖,最适生长和产孢氮源均为蛋白胨,最适生长及产孢温度为28℃,最适pH为6.0,同时菌株Q-1的孢子对紫外线具有一定的耐受力;化学农药中四螨嗪等杀虫剂对菌株Q-1生长影响较小,多菌灵、咪鲜胺等杀菌剂明显抑制菌株Q-1生长;在1×10⁷孢子/mL浓度下,菌株Q-1对棉铃虫幼虫、家蚕幼虫及柑橘全爪螨雌成螨的LT₅₀分别为4.08、21.37和28.43 h。综上,菌株Q-1生长快、产孢量高,对棉铃虫幼虫、家蚕幼虫及柑橘全爪螨雌成螨致病力高,本研究为赭绿青霉进一步开发利用提供理论依据。     

Shikonin inhibits neuronal apoptosis induced by OGD through targeting PI3K/Akt signaling pathway

AIM: To explore the effect of shikonin on rat primary cortical neurons in oxygen-glucose deprivation (OGD)-induced injury model.METHODS: The neurons were pretreated with shikonin at different concentrations (0.02, 0.2, 2 and 20 μmol/L) followed by treatment with OGD. Lactate dehydrogenase (LDH) release assay and fluorescein diacetate/propidium iodide (FDA/PI) double staining were used to detect neuronal viability and apoptosis, and then the optimal concentration of shikonin was determined. LY294002 (PI3K/Akt signaling pathway inhibitor, 1 μmol/L) was added before the addition of shikonin, and the protein level of p-Akt (Ser473) in the neurons was determined by Wes-tern blot. LDH release assay and FDA/PI double staining were also used to detect neuronal viability and apoptosis.RESULTS: A certain concentration (0.2~20 μmol/L) of shikonin increased the viability of impaired neurons (P<0.05) and the protein level of p-Akt (Ser473) in the neurons (P<0.05). The effect of shikonin on neuronal p-Akt (Ser473) levels and the cell death were blocked by LY294002 (P<0.05).CONCLUSION: A certain concentration of shikonin reduces OGD-induced apoptosis of rat primary cortical neurons by activating PI3K/Akt signaling pathway.     

All-trans retinoic acid attenuates blood-brain barrier injury induced by cerebral ischemia-reperfusion in rats through JNK/P38 MAPK signaling pathway

AIM: To investigate the effect of all-trans retinoic acid (ATRA) on blood-brain barrier after cerebral ischemia-reperfusion (CIR) injury in rats and its possible role mechanism.METHODS: Male SD rats were randomly divided into sham group, model (CIR) group and CIR+ATRA (10, 30 and 90 mg/kg) groups. The rat model of CIR injury was established by MCAO thread occlusion method. After ischemia for 1.5 h and reperfusion for 24 h, the neurological functional behavioral score, cerebral infarction volume, brain water content and Evans blue content were determined. The activity of matrix metalloprotein-9 (MMP-9) was measured by gelatin zymography. The protein levels of claudin-5, occludin, ZO-1, JNK, p-JNK, P38, p-P38 and MMP-9 in the brain tissues were determined by Western blot.RESULTS: Compared with CIR model group, ATRA at 30 mg/kg significantly improved neurological function, and decreased cerebral infarction volume, brain water content, Evans blue content and the degradation of tight junction proteins in ischemic area (P<0.01). The activity and protein expression of MMP-9 in ischemic brain tissue were decreased (P<0.01). The phosphorylation of JNK and P38 was inhibited and the protein levels of p-JNK and p-P38 were decreased (P<0.01).CONCLUSION: ATRA reduces the damage of brain tissue and the destruction of blood-brain barrier induced by CIR in rats. The protective effect may be related to inhibiting the activation of JNK/P38 MAPK signaling pathway and MMP-9.     

Cepharanthine induces autophagy via PI3K/AKT/mTOR signaling pathway in ovarian cancer SKOV3 cells

AIM: To investigate the autophagy of human ovarian cancer SKOV3 cells induced by cepharanthine and to explore its mechanism. METHODS: The effect of cepharanthine on the viability of ovarian cancer SKOV3 cells was measured by CCK-8 assay. The SKOV3 cells were treated with cepharanthine, and then the formation of autophagosome was observed with acridine orange staining under fluorescence microscope. The protein levels of LC3, AKT, p-AKT, mTOR, p-mTOR and GAPDH in the SKOV3 cells treated with cepharanthine were determined by Western blot.RESULTS: Cepharanthine significantly inhibited the viability of ovarian cancer SKOV3 cells in a dose-dependent manner (P<0.05). The number of the intracellular acidic autophagosomes with bright red fluorescence was significantly increased after cepharanthine treatment in the SKOV3 cells. The expression of LC3-Ⅱ in SKOV3 cells was significantly enhanced after cepharanthine treatment. Furthermore, treatment with cepharanthine in the SKOV3 cells also resulted in a significant down-regulation of phosphorylated form of AKT and mTOR (P<0.01), while the total protein level was not changed. Combination of cepharanthine and 3-methyladenine resulted in a substantial decrease in the cell viability compared with using cepharanthine alone.CONCLUSION: Cepharanthine significantly inhibits the growth of human ovarian cancer SKOV3 cells and induces the autophagy, which may be correlated with down-regulation of PI3K/AKT/mTOR signaling pathway.     

Effects of capsaicin on cognitive impairment and mitochondria-associated endoplasmic reticulum membranes in rats with chronic cerebral hypoperfusion

AIM:To observe the effects of capsaicin on cognitive impairment and mitochondria-associated endoplasmic reticulum membranes (MAMs) of hippocampal CA1 area in the rats with chronic cerebral hypoperfusion (CCH), and to investigate the underlying molecule mechanism of cognitive defects induced by ischemia. METHODS:Healthy male Sprague-Dawley (SD) rats(n=48) were randomly divided into sham operation (sham) group,CCH model (CCH) group, capsaicin group,and solvent group, 12 rats in each group. Capsaicin at 2.5 mg/kg was intraperitoneally injected twice a week for 4 weeks, starting on the 7th day after surgery. The rats in solvent group were given the same amount of solvent at the same time and under the same conditions. Morris water maze, object recognition test and open field test were conducted to analyze the cognitive related behavior performance on the 4th week after surgery. The changes of MAMs in the hippocampal CA1 region were observed under transmission electron microscope, the co-localization of the MAMs was observed by immunofluorescence double-labeling, and the expression of mitofusin 2 (Mfn2) in the hippocampal tissue was determined by Western blot.RESULTS:Four weeks after the operation, the behavior tests showed that the cognitive function of CCH rats was impaired compared with sham operation group. Compared with solvent group, spatial learning and memory in capsaicin group was improved significantly. The results of transmission electron microscope and confocal microscope showed that the distance of MAMs in the hippocampal CA1 area of CCH rats was increased compared with sham operation group, and the co-localization of the contacts was decreased (P<0.05). Compared with solvent group, the correlation between the mitochondria and ER in capsaicin group was increased (P<0.05). The protein level of Mfn2 in CCH group was significantly lower than that in sham group (P<0.05). Compared with solvent group, the protein level of Mfn2 in capsaicin group was higher (P<0.05). CONCLUSION:CCH rats showed decreased cognitive function and loosen MAMs. Capsaicin improves the cognitive behavior of CCH rats by up-regulation of MAMs.     

茉莉酸甲酯诱导辣椒抗青枯病与活性氧代谢的关系

为探究茉莉酸甲酯(Methyl Jasmonate,Me JA)诱导辣椒抗青枯病效应与活性氧代谢相关酶的关系,以辣椒易感青枯病品种‘粤红1号’和抗青枯病品种‘辛香8号’幼苗为试验材料,在0.1mmol·L-1 Me JA喷雾处理后12、24、48、72和96 h接种青枯劳尔氏菌(Ralstonia solanacearum),对其进行青枯病病情指数与活性氧代谢相关酶——超氧化酶歧化酶(Superoxide Dismutase,SOD)、过氧化氢酶(Catalase,CAT)、过氧化物酶(Peroxidase,POD)和抗坏血酸过氧化物酶(Ascorbate Peroxidase,APX)活性以及丙二醛(Malondialdehyde,MDA)含量测定及相互关系的分析。结果表明:‘粤红1号’和‘辛香8号’的病情指数随喷Me JA处理时间的推移表现为先降后升,但都低于对照;而诱导效果则相反,Me JA处理对两个辣椒品种幼苗抗性的最适诱导时间均为接种前48 h。接种后0~96 h,Me JA喷雾处理的辣椒幼苗叶片SOD、CAT、POD和APX酶活性均显示先升后降的趋势,且明显高于对照,接种后24~48 h达到最高,而MDA含量则明显低于对照。因此,Me JA可诱导辣椒幼苗抗青枯病,其实现途径可能与提高活性氧代谢相关酶活性和缓解膜脂过氧化有关。