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.

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.

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.

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.

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.

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,

改性沸石H-BEA催化4-苯基丁酸分子内付克反应合成1-萘满酮(英文)

以乙二胺四乙酸二钠(EDTA)、柠檬酸、草酸、酒石酸改性制备了H-BEA,并根据XRD和NH3-TPD对沸石H-BEA进行表征。采用上述改性沸石催化4-苯基丁酸分子内付克反应合成1-萘满酮进行催化剂反应活性评价。实验结果表明,以柠檬酸改性沸石H-BEA具有较高的催化活性。进一步对催化剂用量、反应温度、反应时间等工艺条件优化得到最佳工艺条件,在最佳工艺条件下,产物1-萘满酮产率达到94.3%。

Effect of MeJA and Light on the Accumulation of Betulin and Oleanolic Acid in the Saplings of White Birch (<i>Betula platyphylla</i>Suk.)

In this study, we investigated the effect of different types of light and MeJA treatment on the accumulation of betulin and oleanolic acid in various organs of white birch. Our results showed that betulin and oleanolic were accumulated mainly in the stalk skin. The content of both substances in the stalk skin was significantly affected by seasons with a peak accumulation in August. The content of oleanolic and betulin was significantly decreased in the stem skin treated with 4 types of light (red, yellow, blue and green) compared with the plant with normal illumination. In contrast, oleanolic acid in leaves was increased by 13.28 folds when the white birch was treated with green light. Betulin was increased by 1.959 folds in leaves of white birch treated with blue light. The highest content of betulin and oleanolic acid in various organs of birch with appropriate shading treatment (light transmittance: 50%) was increased by 45.09% and 30.50%, respectively, in comparison with those with non-shading treatment. Content of oleanolic acid and betulin can be significantly improved in various parts of birch after treatment with different concentration of MeJA. The study lays the foundation to metabolic regulation of oleanolic acid and betulin in birch.

BEA沸石后合成金属(Sn,Zr,Hf)改性:结合Lewis和Bronsted酸性进行级联催化

Sn,Zr和Hf等Lewis酸性金属中心改性的沸石是许多生物炼制相关反应(如碳水化合物异构化和呋喃Meerwein-Pondorf-Verley(MPV)还原)中有应用前景的催化剂.在大孔BEA沸石框架中固载上述金属离子得到的催化剂性能良好.然而,制备该类催化剂通常需采用昂贵的有机金属前体,并且需要经历多步制备过程.本文开发了一种简易的固态研磨法,采用简单的无机金属前体,在脱铝BEA沸石中成功掺入了高度分散的、高金属含量(Si/M比为50-75)的孤立Sn,Zr和Hf.在样品焙烧前,采用甲醇处理去除过量的金属,可使孤立金属位点高含量、有效地掺杂在BEA框架中.在改性的BEA沸石中,Lewis酸位点来自于开放的Sn,Zr和Hf孤立金属离子位点;Sn改性的BEA上Lewis酸位点还包括封闭的Sn位点,但开放的Sn位点表现出最高的Lewis酸性.Br?nsted酸性来自于受开放金属位点Lewis酸性金属离子摄动的硅羟基以及与开放金属位点相连的羟基.Sn,Zr,Hf改性的BEA沸石在肉桂醛级联还原醚化反应中表现出较好的催化活性.以异丙醇为溶剂,肉桂醛先在Lewis酸位点上发生MPV还原生成肉桂醇;随后,肉桂醇在Br?nsted酸位点发生醚化反应生成肉桂基丙基醚.其中,Sn改性的BEA沸石表现出最高的催化活性,这是因为其具有最强的Lewis酸性,这对第一步MPV反应至关重要.此外,将本研究中Sn改性优化固态离子交换法用于对不同形貌BEA沸石进行改性以提高其催化性能,结果表明,BEA沸石多级孔结构进一步有利于级联还原醚化反应.

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。

桦木酸通过Wnt/β-catenin信号通路调控瘢痕疙瘩成纤维细胞增殖、侵袭和胶原合成

目的研究桦木酸(betulinic acid,BA)对瘢痕疙瘩成纤维细胞增殖、侵袭和胶原合成的影响并探讨分子作用机制。方法收集临床切除的瘢痕疙瘩组织,采取组织块贴壁法分离培养成纤维细胞。细胞分为3组:空白对照组、二甲基亚砜(dimethyl sulfoxide,DMSO)处理组(溶剂对照组)和BA处理组。细胞计数试剂盒-8(cell counting kit-8,CCK-8)法检测细胞生长。5-乙炔基-2’-脱氧尿苷(5-ethynyl-2’-deoxyuridine,EdU)法检测细胞增殖。流式细胞术检测细胞凋亡。Transwell法测细胞侵袭。荧光素酶报告基因实验检测Wnt/β-catenin信号通路活性。实时定量PCR(real-time quantitative PCR,RT-qPCR)检测c-myc和cyclin D1 mRNA表达。Western blot检测Ⅰ型胶原(Collagen typeⅠ,ColⅠ)、β-catenin、c-myc和cyclin D1蛋白表达。结果与空白对照组和DMSO处理组相比,BA处理组瘢痕疙瘩成纤维细胞增殖降低,细胞凋亡率上升,细胞侵袭水平下降,胶原合成减少,差异有统计学意义(P<0.05)。与空白对照组和DMSO处理组相比,BA处理组瘢痕疙瘩成纤维细胞中Wnt/β-catenin信号通路活性降低,β-catenin、c-myc和cyclin D1表达水平减少,差异有统计学意义(P<0.05)。结论桦木酸通过下调Wnt/β-catenin信号通路抑制瘢痕疙瘩成纤维细胞增殖、侵袭和胶原合成。

白桦脂酸的药理活性及分析检测研究进展

白桦脂酸是一种具有广泛药理活性的天然产物,在医药工业中应用十分活跃。介绍了白桦脂酸的物化性质和其抗肿瘤、抗炎、抗病毒、抑菌、改善血脂功能、抗糖尿病、抗氧化应激活性、抗焦虑等药理活性。综述了近年来中药材、药物制剂、生物细胞等样品中白桦脂酸的分析检测研究进展,以期为白桦脂酸的检测技术及中药相关产品的质量控制提供参考。

白桦脂酸在Va24NKT细胞杀伤胰腺癌细胞中的作用机制研究

目的研究白桦脂酸对Va24NKT细胞杀伤胰腺癌细胞的作用机制。方法从外周血中扩增Va24NKT细胞,同时将不同浓度的白桦脂酸作用于Va24NKT细胞、SW-1990细胞,MTT法检测Va24NKT细胞、SW-1990细胞生长,流式细胞仪检测NKG2D表达,Western blot法检测不同浓度白桦脂酸作用后NKT细胞中P-ERK1/2、ERK1/2的表达。结果白桦脂酸浓度在0.125~2μg/mL时能促进Va24NKT细胞的生长(P<0.05),经白桦脂酸诱导后的Va24NKT细胞NKG2D的表达显著高于对照组(P<0.05),对SW-1990细胞的杀伤活性亦显著高于对照组(P<0.05)。结论白桦脂酸在一定浓度下增强Va24NKT细胞杀伤胰腺癌细胞作用,白桦脂酸促进Va24NKT细胞生长与ERK1/2通路有关。

不同中药单体的急性毒性及抗肿瘤活性评价研究

目的:本研究旨在考察姜黄素、黄芩素、白桦脂酸、白藜芦醇和双氢青蒿素等5种中药单体的急性毒性,并初步探讨不同中药单体的抗肿瘤活性。方法:采用IncuCyte活细胞成像技术检测肿瘤细胞的增殖;采用流式细胞术检测肿瘤细胞凋亡;通过小鼠急性毒性实验初步评价不同中药单体的毒性。取健康8周龄B-NDG雌性小鼠,建立胃癌、结直肠癌和乳腺癌的PDX模型,采用腹腔注射和静脉注射两种给药方式,比较姜黄素、黄芩素、白藜芦醇和双氢青蒿素的抗肿瘤活性。结果:姜黄素、黄芩素、白藜芦醇和双氢青蒿素4种中药单体均有不同程度的抑制肿瘤细胞增殖和促进肿瘤细胞凋亡的作用(P<0.05),其中姜黄素活性最强。急性毒性实验显示,小鼠对黄芩素耐受度最好,姜黄素次之。静脉注射姜黄素在BP0880胃癌PDX模型中体现出了明显的抗肿瘤活性(P<0.05)。结论:在5种中药单体中,姜黄素的抗肿瘤活性最强,且在急性毒性中表现出较高的耐受性。

蓝桉果实化学成分的研究

目的 :研究蓝桉Eucalyptusglobulus果实的化学成分。 方法 :应用硅胶柱层析、SephadexLH 2 0凝胶柱层析等方法进行分离纯化 ,根据理化性质和光谱数据等进行结构鉴定。结果 :从蓝桉果实中分离得到 12个化合物 ,鉴定了其中 5个化合物 :桦木酮酸Ⅰ ,白桦脂酸Ⅱ ,熊果酸Ⅲ ,2α ,3β 二羟基乌苏酸Ⅳ。 结论 :化合物I ,Ⅱ ,Ⅲ ,Ⅳ均为首次从该植物中分离得到。

白桦脂醇、白桦脂酸的研究进展及其前景

白桦脂醇、白桦脂酸属羽扇烷型三萜类化合物,近年来,这两种天然产物及其衍生物在抗艾滋病病毒、抗肿瘤等方面表现出较强生物活性受到广泛关注,已成为当今一个研究热点。本文从白桦脂醇、白桦脂酸的来源、衍生化研究、生物活性以及提取制备等方面对近年来的相关研究进行概括总结,并对其研究前景进行展望。