Betulinic acid protects against ovarian impairment by decreasing F-2 toxin-induced oxidative stress and inflammation associated with the downregulation of p38 expression in mice

F-2 toxin is an estrogenic mycotoxin that causes reproductive disorders in animals.Betulinic acid(BA)is a natural pentacyclic lupane-structure triterpenoid that has diverse pharmacological activities.In this study,the antioxidative and anti-inflammatory effects of BA and its underlying mechanism are explored in F-2 toxin-triggered mouse ovarian damage.We found that BA alleviated the F-2 toxin-induced ovarian impairment by stimulating follicle growth,reducing inflammatory cell infiltration,repairing damaged mitochondria and endoplasmic reticulum.Simultaneously,BA not only reversed F-2 toxin-induced reduction of follicle stimulating hormone(FSH)and luteinizing hormone(LH)levels in the serum,but also restrained the protein expression of the estrogen receptors a(ERa)and ERβ.Moreover,BA restored the balance of F-2 toxin-induced ovarian redox system disorders.Subsequently,we found that 0.25 mg/kg BA played an anti-inflammatory role in the F-2 toxin-induced ovarian impairment by decreasing interleukin-1β(IL-1β).IL-6,and tumor necrosis factor-α(TNF-α)mRNA expression,as well as inhibiting p38 protein expression.These data demonstrated that BA exerts its protective effect on F-2 toxin-induced ovarian oxidative impairment and inflammation by inhibiting p38 expression,which implies a natural product-based medicine to ameliorate F-2 toxin-caused female reproductive toxicity and provides a detoxifying method for food contaminated by mycotoxin.

Betulinic acid-mediating miRNA-365 inhibited the progression of pancreatic cancer

Background:The dilemma of pancreatic cancer treatment has become a global challenge.For this reason,effective,feasible,and new medical methods are currently much-needed.Betulinic acid(BA)has been valued as a potential therapy for pancreatic cancer.However,the mechanism by which BA exerts an inhibitory effect on the development of pancreatic cancer remains elusive.Methods:A rat model and two cell models of pancreatic cancer were established,and the effect of BA on pancreatic cancer was verified in vivo and in vitro by using MTT,Transwell,flow cytometry,RT-PCR,Elisa and immunohistochemistry.At the same time,miR-365 inhibitors were introduced to test whether BA played a role in mediating miR-365.Results:BA can significantly inhibit the proliferation and invasion of pancreatic cancer cells and promote apoptosis.In vivo experiments,BA can significantly lower the number of cancer cells and tumor volume in the rat model of pancreatic cancer.In vitro,it was found that BA inhibited the protein level and phosphorylation level of AKT/STAT3 by mediating the expression of miR365/BTG2/IL-6.Like BA,miR-365 inhibitors also significantly inhibited cell viability and invasion ability,and inhibited the protein level and phosphorylation level of AKT/STAT3 by changing the expression of BTG2/IL-6,and their combination had a synergistic effect.Conclusion:BA inhibits AKT/STAT3 expression and phosphorylation by modulating miR-365/BTG2/IL-6 expression,and BA inhibits the progression of pancreatic cancer through the aforementioned mechanism.

Effects of Betulinic Acid on Proliferation and Apoptosis in Jurkat Cells and Its In Vitro Mechanism

The anti-cancer effects of betulinic acid （BA） on Jurkat cells and its in vitro mechanism were examined by using MTT assay. Apoptosis was detected by using Hoechst33258 staining and annexin-Ⅴ/PI double-labeled cytometry. The effects of betulinic acid on the cell cycle of Jurkat cells were studied by propidium iodide method. RT-PCR and Western blotting were used to analyze the changes of cyclin D3, bcl-xl mRNA and protein levels in Jurkat cells after treatment with betulinic acid. Our results showed the proliferation of Jurkat cells was decreased in betulinic acid-treated group with a 24-h IC50 value being 70.00 μmol/L. Betulinic acid induced apoptosis of Jurkat cells in a time-and dose-dependent manner. The number of Jurkat cells treated with betulinic acid showed an increase in G0/G1 phase and decrease in S phase. After treatment with 0, 20, 60, 100 μmol/L betulinic acid for 24 h, the number of Jurkat cells was increased from （31.00±1.25）% to （58.84±0.32）% in G0/G1 phase, whereas it was decreased from （61.45±1.04）% to （35.82±1.95）% in S phase. PBMCs were less sensitive to the cytotoxicity of betulinic acid than Jurkat cells. The expressions of cyclin D3, bcl-xl mRNA and protein were decreased sharply in Jurkat cells treated with betulinic acid. It is concluded that betulinic acid is able to inhibit the proliferation of Jurkat cells by regulating the cell cycle, arrest cells at G0/G1 phase and induce the cell apoptosis. The anti-tumor effects of betulinic acid are related to the down-regulated expression of cyclin D3 and bcl-xl.

Down-regulation of NOX4 by Betulinic Acid Protects against Cerebral Ischemia-reperfusion in Mice

Ischemic stroke leads to high potentiality of mortality and disability. The current treatment for ischemic stroke is mainly focused on intravenous thrombolytic therapy. However, ischemia/reperfusion induces neuronal damage, which significantly influences the outcome of patients with ischemic stroke, and the exact mechanism implicated in ischemia/reperfusion injury remains unclear, although evidence shows that oxidative stress is likely to be involved. Betulinic acid is mainly known for its anti-tumor and anti-inflammatory activities. Our previous study showed that betulinic acid could decrease the reactive oxygen species（ROS） production by regulating the expression of NADPH oxidase. Thus, we hypothesized that betulinic acid may protect against brain ischemic injury in the animal model of stroke. Focal cerebral ischemia was achieved by using the standard intraluminal occlusion method and reperfusion enabled after 2 h ischemia. Neurological deficits were scored. Infarct size was determined with 2,3,5-triphenyltetrazolium chloride monohydrate（TTC） staining and the mRNA expression of NADPH oxidase 4（NOX4） was determined by RT-PCR in infarct tissue. ROS generation and apoptosis in ischemic tissue were analyzed by measuring the oxidative conversion of cell permeable 2＇,7＇-dichloro-fluorescein diacetate（DCF-DA） to fluorescent dichlorofluorescein（DCF） in fluorescence microplate reader and TUNEL assay, respectively. In Kunming mice, 2 h of middle cerebral artery（MCA） occlusion followed by 24 or 72 h of reperfusion led to an enhanced NOX4 expression in the ischemic hemisphere. This was associated with elevated levels of ROS generation and neuronal apoptosis. Pre-treatment with betulinic acid（50 mg/kg/day for 7 days via gavage） prior to MCA occlusion prevented the ischemia/reperfusion-induced up-regulation of NOX4 and ROS production. In addition, treatment with betulinic acid could markedly blunt the ischemia/reperfusion-induced neuronal apoptosis. Finally, betulinic acid reduced infarct volume and ameliorated the neurological deficit in this stroke mouse model. Our results suggest that betulinic acid protects against cerebral ischemia/reperfusion injury in mice and the down-regulation of NOX4 may represent a mechanism contributing to this effect.

Lactic Acid Reduces LPS-Induced TNF-a and IL-6 mRNA Levels Through Decreasing I?Ba Phosphorylation

This study explored the effects over time of lactic acid （LA） on IκBα phosphorylation and nuclear factor-kappa B （NF-κB） p65 protein expression, and on tumor necrosis factor a （TNF-α） and interleukin-6 （IL-6） mRNA levels in rat intestinal mucosa microvascular endothelial cells （RIMMVECs） stimulated by lipopolysaccharide （LPS）. I？Ba, phosphorylated IκBa （p-IκBa） and p65 protein levels were monitored by Western blot analysis, and TNF-a and IL-6 mRNA levels were analyzed using real-time PCR. LA treatment reduced TNF-a and IL-6 mRNA levels in LPS-stimulated RIMMVECs, with the greatest effect being after 3 h. The highest inhibitory effect of LA on IκBa phosphorylation to prevent activation of NF-κB was after 6 h. These results suggest that LA reduces TNF-a and IL-6 mRNA levels through decreasing IκBa phosphorylation and blocking the dissociation of IKK complex, which prevents activation of NF-κB.

Structure and Anti-HIV Activity of Betulinic Acid Analogues

Firstly discovered in 1980s, human immunodeficiency virus （HIV） continues to affect more and more people. However, there is no effective drug available for the therapy of HIV infection. Betulinic acid existing in various medicinal herbs and fruits exhibits multiple biological effects, especially its outstanding anti-HIV activity, which has drawn the attentions of many pharmacists. Among the derivatives of betulinic acid, some compounds exhibited inhibitory activities at the nanomolar concentration, and have entered phase II clinical trials. This paper summarizes the current investigations on the anti-HIV activity of betulinic acid analogues, and provides valuable data for subsequent researches.

Biological Activity of Betulinic Acid: A Review

Betulinic acid is a known natural product which has gained a lot of attention in the recent years since it exhibits a variety of biological and medicinal properties. This review provides the most important biological properties of betulinic acid.

A 3D Ba(Ⅱ) Inorganic-organic Hybrid Framework Based on 1,3,5-Benzenetricarboxylic Acid Ligand: Synthesis and Characterization

A three-dimensional（3D） barium complex with 1,3,5-benzenetricarboxylic acid（H3BTC）, {[Ba1.5（BTC）（H2O）]·（H2O）}n（1）, was synthesized in DMF/EtOH/H2O mixed solution under solvothermal conditions, and characterized by single-crystal X-ray diffraction, elemental analyses, IR spectra, thermogravimetric analyses, and photoluminescence measurement. In complex 1, the 2D I2O0 type inorganic layer is constructed by {Ba1O10} and {Ba2O9} polyhedra. Moreover, the solid-state fluorescence measurement reveals a fluorescence emission band at 465 nm under 344 nm excitation, assigned to a charge-transfer transition.

Inhibition of betulinic acid to growth and angiogenesis of human colorectal cancer cell in nude mice

Objective： Angiogenesis plays a major role in the pathogenesis of many disorders. Vascular endothelial growth factor （VEGF） has been shown to be the key regulator of normal and pathological angiogenesis. Many studies showed that decreased expression of VEGF has been inhibited growth and migration of cancer cells. The aim of this study was to explore the effects of Betulinic acid on the VEGF expression and the growth of colorectal cell SW480 xenografts in nude mice. Methods： The xenografts derived from colorectal cell SW480 were established in BALB/C nude mice. Inoculated mice were randomly divided into negative control （corn oil）, low dose betulinic acid group （20 mg/kg/d） and high dose group （40 mg/kg/d）. After 22 days, the animals were sacrificed; tumor volume and weights were measured. The mRNA level of VEGF was analyzed by quantitative real-time polymerase chain reaction. The expression of VEGF protein was detected by immunohistochemistry. Results： The tumor weight was significantly lower in low and high dose groups than in corn oil group （1.12 ＋ 0.04, 0.43 ＋ 0.02 vs 2.08 ＋ 0.07; P 〈 0.05）. The mRNA levels of VEGF was also significantly lower in betulinic acid treated groups （0.72 ＋ 0.02, 0.38 ＋ 0.01; P 〈 0.05） than in control group （1.08 ＋ 0.04）. H＆E staining showed tumor tissue necrosis was observed in treatment groups. The positive expression of VEGF was lower in low and high dose groups than in corn eil group. Gray scale increased in low dose group and high dose group （121.1 ＋ 2.8, 156.2 ＋ 3.3, P 〈 0.05）. Conclusion： Betulinic acid had significant inhibitory effect on VEGF expression and tumors growth of human colorectal cancer xenografts in vivo, and down-regulation of VEGF expression may account for one of the molecular mechanisms of the anticancer effects of betulinic acid.

RT-PCR/CRISPR-Cas12a快速检测和区分SARS-CoV-2 Omicron BA.4/5变异株

目的建立一种基于CRISPPR-Cas12a基因编辑技术对新型冠状病毒(SARS-CoV-2)奥密克戎BA.4/5变异株快速检测与鉴别的方法。方法结合逆转录聚合酶链式反应(RT-PCR)与CRISPR基因编辑技术,基于次优原间隔区相邻基序(suboptimal-PAM)设计奥密克戎BA.4/5变异株特异性的CRISPRRNA(crRNA),从而建立RT-PCR/CRISPR-Cas12a快速检测新冠病毒BA.4/5变异株的方法。本研究检测了43例新冠病毒阳性的临床样本(包括新冠病毒野生株以及变异株Alpha、Beta、Delta、奥密克戎BA.1和BA.4/5)以及20例新冠病毒阴性的临床样本(包括11种常见呼吸道病原体),并以测序结果为金标准计算PCR/CRISPR-Cas12a检测方法的ROC曲线下面积(AUC)以及灵敏度(SEN)、特异性(SPE)、一致性(Kappa)评价检测方法的性能。结果本研究筛选到两条特异性crRNA-1和crRNA-2,所建立的方法可在30min内快速特异地检测出SARS-CoV-2奥密克戎BA.4/5变异株,最低检测限为10copies/μL。此外,在检测感染11种常见呼吸道病原体的临床样本时均未观察到非特异性交叉反应。基于crRNA-1和crRNA-2的检测结果的灵敏度分别为97.83%、100%;特异性均为100%;ROC曲线下面积分别为0.9989和1.0;与Sanger测序方法的一致性分别为92.83%、96.41%。结论本研究采用CRISPPR-Cas12a基因编辑技术与逆转录聚合酶链式反应相结合,成功建立了一种快速检测与鉴别SARS-CoV-2奥密克戎BA.4/5变异株的新方法。其特异性强、灵敏度高、稳定性好,可用于新冠病毒奥密克戎BA.4/5变异株的批量检测与分型,可用于常规监测和跟踪SARS-CoV-2变异的传播。

Antitumor Effect of Betulinic Acid on Human Acute Leukemia K562 Cells in vitro

The effects of betulinic acid (BA), a pentacyclic lupane-type triterpene, on the cell viability, cell cycle and apoptosis in human leukemia K562 cells were investigated. The effects of BA on the growth of K562 cells were studied by MTT assay. Apoptosis was assayed through Annexin V/propidium iodide (PI) double-labeled cytometry. The effects of BA on the cell cycle of K562 cells were studied by a PI method. The expression of Bax and capase-3 was detected by using Western blot. The results showed that BA was cytotoxic to K562 cells with an IC50 of 21.26 μg/mL at 24 h. After treating K562 cells with 10 μg/mL BA for 72 h, the number of cells was reduced by 58%. BA induced apoptosis of K562 cells in a time-and dose-dependent manner. The proportion of cells in G0/G1 and G2/M phases was decreased and that in S phase was increased after K562 cells were treated with BA for 24 h. BA treatment also increased the expression of the pro-apoptotic proteins Bax and caspase-3. It suggested that BA could inhibit the proliferation of K562 cells through the induction of cell cycle arrest and apoptosis. The antitumor effects of BA were related with up-regulation of the expression of Bax and caspase-3 proteins. BA may qualify for the development of new therapies for leukemia.

Cytotoxic Activity of Betulinic Acid Derivatives Synthesized Using Enzymes

Betulinic acid, a triterpenoid found in many plant species, has attracted attention due to its important pharmacological properties, such as anti-cancer and anti-HIV activities. In order to obtain derivatives potentially useful for detailed pharmacological studies, betulinic acid derivatives were synthesized by reaction of betulinic acid with benzoyl chloride and with acetic anhydride using lipase as catalyst. Enzyme-catalyzed of betulinic acid with benzoyl chloride converted betulinic acid into 3β-benzoil-lup-20（29）-ene-28-oic acid ester （BCL） whereas with acetic anhydride converted betulinic acid into 3β-acetoxy-lup-20（29）-ene-28-oic acid ester （BAA）. The BAA then underwent further reaction with l-decanol to produce 3β-acetoxy-lup-20（29）-ene-28 decanoate （BAAD）. Betulinic acid derivatives prepared were tested for cytotoxic activity on three cancer cell lines in vitro： all tested compounds showed stronger cytotoxic activity than betulinic acid,

6-BA Gibberellic Acid 3.6% Liquid HPLC Analysis Method Research

本文采用高效液相色谱法，以甲醇＋甲酸水溶液为流动相，使用ODSC18、51μm为填料的不锈钢柱和二极管阵列检测器。在210nm波长下对赤霉酸·6-BA进行分离和定量分析。结果表明，该分析方法的线性相关系数赤霉酸为O．9999；6-BA为0．998；标准偏差赤霉酸为0．01；6-BA为0．02；变异系数赤霉酸为0．46％；6-BA为0．30％；赤霉酸平均回收率为97．7％；6-BA平均回收率为98．7％。

Bifidobacterium longum CCFM1077 Attenuates Hyperlipidemia by Modulating the Gut Microbiota Composition and Fecal Metabolites:A Randomized,Double-Blind,Placebo-Controlled Clinical Trial

An increasing number of studies have indicated that gut microbiota and its metabolites are crucial in the development of hyperlipidemia.Bifidobacterium longum(B.longum)CCFM1077 has been shown to have lipid-lowering effects in animals.This study aimed to evaluate the potential of B.longum CCFM1077 in lowering the lipid levels in patients with hyperlipidemia and investigate the effect of this bacterium on serum lipid abnormalities,gut microbiota,and fecal metabolites in these patients.This study was a six-week,randomized,double-blind,and placebo-controlled pilot clinical trial.Subjects with hyperlipidemia(N=62)were randomly assigned to receive placebo(N=31)or B.longum CCFM1077(1×1010colony-forming units(CFUs)per day;N=31).Serum lipid levels including total cholesterol(TC),lowdensity lipoprotein cholesterol(LDL-C),total triglyceride(TG),and high-density lipoprotein cholesterol(HDL-C)were examined at the baseline and interventio nal endpoints.Changes in the gut microbiota composition and diversity were measured based on 16S ribosomal RNA(rRNA)sequencing of the V3-V4region at the end of the intervention period.Non-targeted metabolomics of the feces was performed using ultra-performance liquid chromatography(UPLC)-Q-Exactive Orbitrap/mass spectrometer.Oral administration of B.longum CCFM1077 for six weeks significantly decreased the serum levels of TC(p<0.01)and LDL-C(p<0.01)in patients with hyperlipidemia.B.longum CCFM1077 treatment markedly increased gut microbiota diversity and the relative abundance of anti-obesity-related genera,including Lactobacillus,Butyricicoccus,Bifidobacterium,and Blautia,whereas it decreased the relative abundance of obesity-related genera,including Alistipes,Megamonas,and Catenibacterium.Additionally,some key metabolites(bile acids(BAs),biotin,and caffeine)and their corresponding metabolic pathways(primary BA biosynthesis,and taurine and hypotaurine,biotin,purine,and caffeine metabolisms)were enriched by B.longum CCFM1077,and thus it may lower lipid levels.B.longum CCFM1077 is a probiotic strain with the potential to lower serum TC and LDL-C levels patients with hyperlipidemia.The underlying mechanism may be related to the increased abundance of anti-obesity-related genera and fecal metabolites.These findings provide a foundation for future clinical applications of lipid-lowering probiotics in managing individuals with hyperlipidemia.

白桦脂酸通过RRAGD/mTOR/ULK1促进自噬改善血管平滑肌细胞钙化

目的 探讨白桦脂酸(Betulinic acid, BA)对高磷诱导血管平滑肌细胞钙化的作用机制。方法 采用2.6μmol·g^(-1)高磷诱导小鼠主动脉平滑肌细胞体外钙化模型,CCK8检测白桦脂酸对细胞活力的影响;加入白桦脂酸低、中、高剂量(5μmol·L^(-1)、10μmol·L^(-1)、20μmol·L^(-1))及自噬抑制剂3-甲基腺嘌呤(3-MA,5μmol·g^(-1))。慢病毒过表达Ras相关GTP结合蛋白D(Ras-related GTP-binding Protein D,RRAGD)转染血管平滑肌细胞,通过荧光显微镜、RT-PCR验证转染效率。采用茜素红染色、细胞内钙含量、碱性磷酸酶活性检测细胞钙化程度;Western blot检测血管平滑肌细胞钙化指标RUNT相关转录因子2(Runt-related transcription factor 2,RUNX2),骨形态发生蛋白2(Bone morphogenetic protein, BMP2),平滑肌蛋白22α(Smooth muscle protein 22α,SM22α)和平滑肌肌动蛋白(α-smooth muscle actin, α-SMA);UNC-51样激酶1(UNC-51-like kinase 1,ULK1),自噬蛋白微管相关蛋白1轻链3(LC3Ⅱ/LC3Ⅰ),泛素结合蛋白P62(P62),哺乳动物雷帕霉素靶蛋白(Mammalian target of rapamycin, mTOR)以及RRAGD的表达。结果 根据CCK8细胞活力结果选择白桦脂酸5、10、20μmol·L^(-1)剂量进行后续实验;钙水平、碱性磷酸酶活性及茜素红染色实验结果显示白桦脂酸改善高磷诱导血管平滑肌细胞钙化;Western blot结果显示白桦脂酸下调RUNX2、BMP2、RRAGD、p-mTOR、P62(P<0.05),上调SM22α、α-SMA、LC3Ⅱ/Ⅰ、p-ULK1的蛋白表达(P<0.05)。白桦脂酸减轻高磷诱导血管平滑肌细胞钙化的作用被自噬抑制剂3-MA和过表达RRAGD阻断。结论 白桦脂酸可能通过RRAGD/mTOR/ULK1信号通路促进自噬抑制血管平滑肌细胞钙化。

桦木酸对右旋糖酐硫酸钠诱导的小鼠结肠炎的保护作用

目的:研究桦木酸(betulinic acid,BA)对右旋糖酐硫酸钠(dextran sodium sulfate,DSS)诱导结肠炎的影响。方法:将84只C57BL/6小鼠随机分为7组,即对照组,BA组(0.5 mg/kg),DSS组(质量分数4%),BA低、中、高剂量(0.25、0.5、1 mg/kg)+DSS组,5-氨基水杨酸(5-aminosalicylic acid,5-ASA)(50 mg/kg)+DSS组。BA或5-ASA连续灌胃14 d,从第8天开始每天饮用4%DSS水溶液,连续7 d诱导小鼠结肠炎,随后测量小鼠结肠长度,苏木精&伊红染色和透射电镜观察结肠病理变化与超微结构,免疫荧光染色法检测活性氧(reactive oxygen species,ROS)水平,实时聚合酶链式反应仪检测结肠炎性因子水平以及TUNEL染色检测细胞凋亡。结果:DSS诱导结肠的长度显著缩短(P<0.05),肠道隐窝排列紊乱且表面不规则,杯状细胞数量减少,肠道紧密连接不完整,微绒毛稀疏;同时,DSS诱导ROS累积和炎性因子白细胞介素-1β(interleukin-1β,IL-1β)、IL-6和IL-10 mRNA水平极显著性上调(P<0.01),下调肿瘤坏死因子-αmRNA的表达(P<0.01),促进细胞凋亡(P<0.01)。然而,BA或5-ASA预处理均能逆转这一趋势,并且BA的作用效果优于5-ASA。结论:BA通过改善肠道结构的完整性,减少ROS产生和改善炎症反应,抑制细胞凋亡,从而对DSS诱导的结肠炎具有预防性的保护作用。

6-BA对葡萄果实中有机酸积累及相关基因表达的影响

为探究6-BA对葡萄果实中有机酸积累的影响,及其调控果实有机酸合成的分子机制,以里扎马特葡萄为试材,花前5 d、花后3 d和花后10 d连续3次对花序与果穗进行6-BA处理,研究6-BA对葡萄果实中有机酸积累及其代谢相关基因表达的影响。结果表明,成熟果实中有机酸含量与6-BA处理浓度密切相关,30 mg/L处理后,成熟果实中的酒石酸和总酸含量均显著低于对照,但对苹果酸、柠檬酸和草酸含量并未产生较大影响;对于10,20 mg/L 6-BA处理而言,处理与对照成熟果实中的各种有机酸含量均不存在显著差异。基因表达结果表明,6-BA处理对IDH、MDH和PEPC基因的表达总体表现为抑制,但对于ME基因的表达则主要表现为促进。据此分析,6-BA处理抑制果实中有机酸合成的原因可能与其影响部分有机酸代谢相关基因的表达有关。

施硒和6-BA对葡萄叶片衰老与活性氧代谢的影响

【目的】明确氨基酸硒和6-BA对葡萄叶片衰老与活性氧代谢的影响,为延缓叶片衰老技术的提出提供理论依据。【方法】以设施延迟栽培条件下叶片衰老速度不同的‘意大利’和‘无核白鸡心’2个葡萄品种为试材,分别进行叶面喷施氨基酸硒和6-BA处理,以喷施等量清水作为对照,研究施硒及6-BA对叶片衰老期间各功能叶片的叶绿素含量、净光合速率(Pn)、丙二醛(MDA)含量和超氧阴离子自由基(O2·)、过氧化氢(H2O2)含量及过氧化氢酶(CAT)、过氧化物酶(POD)、超氧化物歧化酶(SOD)抗氧化酶活性的影响。【结果】与对照相比,外源氨基酸硒和6-BA处理显著延缓了叶片的叶绿素含量和净光合速率(Pn)的下降,提高了过氧化氢酶(CAT)、过氧化物酶(POD)、超氧化物歧化酶(SOD)的活性,从而减慢了丙二醛(MDA)、超氧阴离子自由基(O2·)、过氧化氢(H2O2)的上升速率,延缓了叶片衰老。2个品种间比较,‘意大利’叶片衰老缓慢,在生育后期仍能维持较高的抗氧化酶活性。【结论】氨基酸硒和6-BA处理可有效提高叶片的抗衰老能力,延长叶片的功能期。

6-BA对葡萄果实生长及碳、氮同化物运输的影响

研究了 6 BA对葡萄果实生长及碳、氮同化物运输、分配的影响。结果表明 ,果穗浸蘸 10 0或2 0 0mg/L 6 BA ,均可明显提高坐果率 ,对果粒大小、可溶性固形物含量影响较小。 6 BA处理 14 CO2 饲喂叶 ,抑制了饲喂叶 14 CO2 同化物的输出 ,但 6 BA处理饲喂叶上方正在生长的“库叶” ,则增加了饲喂叶同化物的输出。 6 BA在盛花和盛花后 10d浸蘸花序 2次 ,增加了饲喂叶 14 CO2 、 14 C -谷氨酸 ( 14 C Glu)向穗轴及果实的输入。

6-BA及氨基酸硒对葡萄叶片衰老的影响

【目的】明确6-BA及氨基酸硒在激素水平上对葡萄叶片衰老的调控,为设施葡萄叶片衰老延缓技术的建立提供理论依据。【方法】在设施葡萄延迟栽培条件下,以叶片衰老速度不同的‘意大利’和‘无核白鸡心’2个葡萄品种为试材,分别进行叶面喷施6-BA和氨基酸硒处理,以清水为对照,测定不同处理和对照叶片衰老期间功能叶片的叶绿素含量和净光合速率(Pn)及内源激素含量与比值的变化。【结果】外源6-BA和氨基酸硒处理显著延缓了叶片叶绿素含量和净光合速率的下降,明显提高了玉米素核苷(ZR)和赤霉素(GA3)含量和ZR/ABA(脱落酸)、GA3/ABA、(ZR+GA3)/ABA比值,显著降低了ABA含量。生长素(IAA)具有前期保持叶片生长发育和后期促进衰老的双重作用。2个葡萄品种间比较,‘意大利’叶片衰老缓慢。【结论】6-BA和氨基酸硒通过维持较高的GA3/ABA、ZR/ABA和(GA3+ZR)/ABA比值,提高了葡萄叶片的叶绿素含量和净光合速率,延长了功能期,因此,外源喷施6-BA和氨基酸硒是延缓葡萄叶片衰老的重要技术措施。