Tetracyclic Quinolizidine Alkaloids Research Articles

Preventive effects of matrine on LPS-induced inflammation in RAW 264.7 cells and intestinal damage in mice through the TLR4/NF-κB/MAPK pathway

BackgroundMatrine is a tetracyclic quinolizidine alkaloid with diverse bioactive properties, including anti-inflammatory and neuroprotective properties. However, the underlying anti-inflammatory mechanisms remain unclear. PurposeThis study aimed to explore how matrine reduces Lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 cells and to assess its protective effects against LPS-induced intestinal damage. MethodsThe effect of matrine on cell viability was assessed using the cell counting kit-8 (CCK-8) assay. Additionally, its impact on inflammatory cytokines and macrophage polarization was assessed using enzyme-linked immunosorbent assay (ELISA), flow cytometry, and quantitative real-time polymerase chain reaction (qRT-PCR) analyses. The effects on intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), nitric oxide (NO) production, and oxidative stress were evaluated using 2′,7′-dichlorodihydrofluorescein diacetate staining and JC-1 and Griess assays. Immunofluorescence staining was used to observe the translocation of the NF-κB p65 subunit. Western blotting (WB) and qRT-PCR were employed to analyze the expression levels of proteins related to the toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB)/mitogen-activated protein kinase (MAPK) pathway. An LPS-induced mouse model was established to study the intestinal inflammation and barrier injury. Mouse feces characteristics, colon length, and disease activity index (DAI) were recorded. Hematoxylin-eosin (H&E) and alcian blue/periodic acid schiff (AB/PAS) staining were used to observe morphological changes and barrier damage in the duodenum, jejunum, ileum, and colon and to measure villus length, crypt depth, goblet cell count, and positive areas in the duodenum, jejunum, and ileum. The content of short-chain fatty acids (SCFAs) in the colon was determined using gas chromatography (GC). ResultsMatrine inhibited LPS-induced inflammatory cytokine levels, suppressed macrophage M1 polarization, and promoted M2 macrophage polarization. Matrine reduced LPS-induced increases in ROS and NO levels and regulates oxidative stress. Additionally, matrine inhibited the nuclear translocation of the NF-κB p65 subunit and exerted anti-inflammatory effects by suppressing the activation of the TLR4/NF-κB/MAPK pathway. In vivo experiments indicated that matrine significantly alleviated LPS-induced diarrhea, increased DAI, and shortened the colon. Matrine reduced the production of the pro-inflammatory cytokine interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α and the pro-inflammatory mediator NO in mouse intestinal tissues while promoting the content of the anti-inflammatory cytokine IL-10. Furthermore, it improved intestinal tissue structure and alleviated LPS-induced intestinal barrier damage. Finally, matrine increased the SCFA levels in the intestine. ConclusionMatrine exerted its anti-inflammatory effects and protects against intestinal injury through the TLR4/NF-κB/MAPK signaling pathway.

Sophocarpine Alleviates Isoproterenol-Induced Kidney Injury by Suppressing Inflammation, Apoptosis, Oxidative Stress and Fibrosis.

One of the most common diseases affecting people and leading to high morbidity is kidney injury. The alleviation of inflammation and apoptosis is considered a potential therapeutic approach for kidney injury. Sophocarpine (SOP), a tetracyclic quinolizidine alkaloid, exhibits various beneficial biological properties. To investigate the effects of SOP on isoproterenol (ISO)-induced kidney injury, we randomly divided mice into four groups: Control, ISO, ISO+SOP (20 mg/kg) and ISO+SOP (40 mg/kg). SOP was administered intraperitoneally to the mice over two weeks, accompanied by intraperitoneal stimulation of ISO (10 mg/kg) for another four weeks. After the mice were sacrificed, several methods such as ELISA, staining (H&E, TUNEL, DHE and Masson) and Western blotting were applied to detect the corresponding indicators. The kidney injury serum biomarkers SCr and BUN increased after the ISO challenge, while this effect was reversed by treatment with SOP. Pathological changes induced by ISO were also reversed by treatment with SOP in the staining. The inflammatory cytokines IL-β, IL-6, TNF-α, MCP-1 and NLRP3 increased after the challenge with ISO, while they were decreased by treatment with SOP. The apoptotic proteins cleaved-caspase-3 and Bax increased, while Bcl-2 decreased, after the challenge with ISO, and these effects were reversed by treatment with SOP. The antioxidant proteins SOD-1 and SOD-2 decreased after being stimulated by ISO, while they increased after the treatment with SOP. The fibrotic proteins collagen I, collagen III, α-SMA, fibronectin, MMP-2 and MMP-9 increased after the challenge with ISO, while they decreased after the treatment with SOP. We further discovered that the TLR-4/NF-κB and TGF-β1/Smad3 signaling pathways were suppressed, while the Nrf2/HO-1 signaling pathway was activated. In summary, SOP could alleviate ISO-induced kidney injury by inhibiting inflammation, apoptosis, oxidative stress and fibrosis. The molecular mechanisms were suppression of the TLR-4/NF-κB and TGF-β1/Smad3 signaling pathways and activation of the Nrf2/HO-1 signaling pathway, indicating that SOP might serve as a novel therapeutic strategy for kidney injury.

Analgesic and Anti-Inflammatory Activities of Sophocarpine from Sophora viciifolia Hance.

Sophora viciifolia Hance is an edible plant used in traditional Chinese medicine. Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora viciifolia Hance. Here, we study the analgesic and anti-inflammatory effects, as well as the acute toxicity of sophocarpine from Sophora viciifolia Hance in mice. Sophocarpine (20, 40, and 80 mg/kgbw) significantly prolonged the delay period before a hot plate reaction occurred (all P < 0.05), and the delay before a tail-flick response was induced by a warm bath (P < 0.05; P < 0.01). Sophocarpine (40, 80 mg/kg) resulted in dose-dependent inhibition of the writhing reaction induced by acetic acid in mice (P < 0.05; P < 0.001, respectively). Sophocarpine (80 mg/kg) reduced the total duration of a formalin-induced pain response (P < 0.05). Sophocarpine prolonged the foot-licking latency of mice after the hot plate reaction, and this effect was antagonized by calcium chloride and enhanced by verapamil. Sophocarpine (20, 40, and 80 mg/kg) significantly inhibited xylene-induced ear edema (P < 0.01; P < 0.001; P < 0.001, respectively) and the penetration of acetic acid-induced dye into the peritoneal cavity (P < 0.01; P < 0.01; P < 0.001, respectively). It also reduced the levels of proinflammatory cytokine interleukin (IL)-1β, IL-6, and prostaglandin E2 (P < 0.05, P < 0.01, P < 0.001) and those of serum nitric oxide (P < 0.05). The results of this study suggest that sophocarpine possesses certain analgesic and anti-inflammatory activities, which may be related to calcium and inhibition of the secretion of inflammatory factors.

Anti-cancer potential of sophoridine and its derivatives: Recent progress and future perspectives.

Cancer is the second leading cause of mortality and has resulted in about 9.6 million deaths around the world in 2018. Cancer-caused deaths are expected to be 11.5 million by 2030 all over the world. Because of the fatal nature of cancer, substantial efforts are made all over the world to combat it. Phytoconstituents such as certain alkaloids, saponins, tannins, polyphenols, and terpenoids exhibit anticancer effects. Sophoridine is a tetracyclic quinolizidine alkaloid isolated from the stem and leaves of medicinal plants Sophora alopecuroides L., and Euchresta japonica Benth, and roots of Sophora alopecuroides Ait. Chinese Food and Drug Administration (CFDA) approved sophoridine as an antitumor agent in 2005. This review covers the antitumor activities of sophoridine and its derivatives. The efficacy of sophoridine analogs is expressed with respect to their half-maximal inhibitory concentration (IC50 values). Structure-activity relationship (SAR) study for most of the sophoridine derivatives has been explained. Moreover, the current market of anticancer drugs and its expected growth are discussed. Prospects provide suggestions and clues for novel sophoridine-based anticancer agents with enhanced expected efficacy and minimum toxicity.

Protective effect of sophocarpine on lipopolysaccharide-induced acute lung injury in mice

Sophocarpine (SOP) is a tetracyclic quinolizidine alkaloid isolated from Sophora alopecuroides L. A number of studies have shown that SOP has anti-inflammatory actions and protects against a variety of tissue and organ injuries. The purpose of this study was to investigate the protective effects of SOP on LPS-induced acute lung injury (ALI) in mice. Lung histological alterations, edema, and MPO activity were measured in this study. Furthermore, the production of inflammatory cytokines and the expression of NF-κB and MAPKs signaling pathways were measured. The results showed that the LPS-induced lung histological alterations, edema, protein concentration, inflammatory cell level in BALF, MDA content, and MPO activity were significantly attenuated by SOP. The LPS-induced inflammatory cytokine TNF-α, IL-1β, and IL-6 were also inhibited by SOP. SOP also inhibited the LPS-induced IL-6 and IL-8 production in A549 cells. Western blot analysis demonstrated that SOP remarkably inhibited the phosphorylation of IκBα and NF-κB. LPS-induced MAPKs activation and TLR4 expression were also suppressed by treatment with SOP. In conclusion, the results indicate that SOP protects against LPS-induced ALI by inhibiting TLR4 signaling pathway.

Targeting miR-21 with Sophocarpine Inhibits Tumor Progression and Reverses Epithelial-Mesenchymal Transition in Head and Neck Cancer

A major challenge for cancer chemotherapy is the development of safe and clinically effective chemotherapeutic agents. With its low toxicity profile, sophocarpine (SC), a naturally occurring tetracyclic quinolizidine alkaloid derived from Sophora alopecuroides L, has shown promising therapeutic properties, including anti-inflammatory, anti-nociceptive, and antivirus activities. However, the antitumor efficacy of SC and its underlying mechanisms have not been completely delineated. In the present study, the inhibitory effect of SC onhead and neck squamous cell carcinoma (HNSCC) progression and possible mechanisms for this effect involving microRNA-21 (miR-21) regulation were investigated. By cell viability, Transwell, and wound healing assays, we show that SC effectively inhibited proliferation, invasion, and migration of HNSCC cells. Moreover, SC exerted its growth-inhibitory effect via the downregulation of miR-21 expression by blocking Dicer-mediated miR-21 maturation. Furthermore, SC treatment led to the increased expression of PTEN and p38MAPK phosphorylation as well as the reversal of epithelial-mesenchymal transition (EMT), which was rescued by ectopic expression of miR-21 in cells. Notably, SC dramatically repressed tumor growth without observable tissue cytotoxicity in a mouse xenograft model of HNSCC. Our findings offer a preclinical proof of concept for SC as a leading natural agent for HNSCC cancer therapy.

ПРОТИВОВИРУСНАЯ АКТИВНОСТЬ СУММЫ АЛКАЛОИДОВ GENISTA TINCTORIA И ЕЕ ОТДЕЛЬНЫХ ФРАКЦИЙ В ОТНОШЕНИИ ВИРУСА ГРИППА А(H1N1)PDM09

The ability of alkaloids of the aerial part of Genista tinctoria L. (a dye dye) collected during the flowering period in the Alsheevsky district of the Republic of Bashkortostan, to inhibit the reproduction of the influenza A (H1N1) virus pdm09 was studied. The component composition of the sum of alkaloids and individual fractions is determined by the chromatography-mass spectrometric method. Cytotoxicity and anti-influenza properties of G. tinctoria alkaloids have been studied in vitro in the culture of MDCK cells with respect to the strain of influenza A / California / 07/09 (H1N1) pdm09, rimantadine was used as the reference preparation. Based on the data obtained, a 50% cytotoxic dose of C50, a 50% inhibitory dose of IC50, and a SI selectivity index characterizing the selectivity of the action of the sample against the virus were calculated. According to the data obtained, fraction 4 of the sum of alkaloids of G. tinctoria (SI = 10), containing alkaloids 12-N-methylcytisine, (-)-cytisin, d-lupanin, 12-N-formylcytisine, anagirine, baptilin, and fraction 5 (SI = 7) containing (-)-cytisin, anagirine and baptiphlin. Anagyrin is a major component of fraction 4, its content is 0.13% of the weight of air-dry raw materials, and baptilin-5, its content is 0.14%. It should be noted that, in comparison with the sum of G. tinctoria alkaloids and fractions 2 and 3, fractions 4 and 5 enriched with tetracyclic quinolizidine alkaloids (anagirine and baptifolin) show more pronounced anti-influenza activity. The revealed regularity can serve as the basis for further optimization of the anti-influenza properties of these alkaloids by means of their chemical transformations.

Rotational spectra of tetracyclic quinolizidine alkaloids: does a water molecule flip sparteine?

Sparteine is a quinolizidine alkaloid used as a chiral auxiliary in asymmetric synthesis. We examine whether hydration by a single molecule can flip sparteine from the most stable trans conformation to the bidentate cis arrangement observed in catalytic complexation to a metal center. Sparteine and the sparteine-water dimer were generated in a supersonic jet expansion with H216O and H218O, and characterized by broadband chirped-pulse microwave spectroscopy. Even though the bidentate water dimer was predicted with larger binding energy, a single isomer was observed for the monohydrated cluster, with sparteine retaining the trans conformation observed for the free molecule. The absence of the bidentate dimer is attributed to the kinetic control of cluster formation, favoring the pre-expansion most abundant monomer. The structural properties of the O-HN hydrogen bond in the dimer are compared with those of complexes of other secondary and tertiary amines.

Sophocarpine attenuates toll‐like receptor 4 in steatotic hepatocytes to suppress pro‐inflammatory cytokines synthesis

Sophocarpine, a tetracyclic quinolizidine alkaloid derived from Sophora alopecuroides L., has been documented that it can suppress pro-inflammatory cytokines synthesis in alleviating nonalcoholic steatohepatitis (NASH) in vivo. Toll-like receptor 4 (TLR4) is a pattern recognition receptor whose activation results in the production of several pro-inflammatory cytokines. It has been reported that TLR4 is upregulated in nonalcoholic fatty liver disease and plays an important role in the pathogenesis of NASH. This study aimed to examine the changes of TLR4 and its signaling pathways in sophocarpine's anti-inflammatory process on experimental NASH in vitro. Primary hepatocytes were isolated, and oleic acid-induced steatosis model was established. Cell Counting Kit-8 assay was used to detect the number of metabolically active mitochondria and viable cells. Immunocytochemistry analysis was applied to evaluating pro-inflammatory cytokines synthesis. Total RNA and protein were extracted for real-time polymerase chain reaction and Western blot detection. Enhanced expression of TLR4 was observed in oleic acid-induced steatotic hepatocytes. Sophocarpine suppressed pro-inflammatory cytokines synthesis and reduced the expression of TLR4 in steatotic hepatocytes. Expression of TLR4 and pro-inflammatory cytokines recovered after sophocarpine was removed. Moreover, sophocarpine restrained the activation of nuclear factor-kappaB (NF-κB), c-Jun-N-terminal kinase (JNK), and Extracellular regulated protein kinases (ERK) signaling pathways in the anti-inflammatory process. Sophocarpine could decrease the expression of TLR4 in steatotic hepatocytes and suppress pro-inflammatory cytokines synthesis. NF-κB, JNK, and ERK signaling pathways were important workable downstream pathways.

Oral sophocarpine protects rat heart against pressure overload-induced cardiac fibrosis

Context: Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides Linn. (Kudouzi). Sophocarpine injection was found to have significant antiviral effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in the clinic.Objective: This study assessed the effects of sophocapine on overload-induced cardiac fibrosis and investigated potential mechanisms.Materials and methods: Adult male Sprague–Dawley rats were subjected to a suprarenal abdominal aorta constriction (AC) or sham to induce sustained pressure overload. Six weeks later, rats were randomly assigned to receive sophocapine (10, 20, and 40 mg/kg, gavage) or vehicle treatment for an additional 6 weeks. Six weeks after treatment, cardiac dysfunction, cardiac coefficient, cardiac fibrosis, hydroxyproline concentration, and inflammation mediators were examined.Results: When compared with the model group, the left ventricular weight/body weight decreased by 25.4% and 39.0% in 20 and 40 mg/kg sophocarpine groups, respectively. The beneficial effects were associated with amelioration of left ventricular systolic pressure (LVSP) and left ventricular enddiastolic pressure (LVEDP). Moreover, pressure overload-induced cardiac fibrosis was attenuated in sophocarpine treated groups. Importantly, sophocarpine (20 and 40 mg/kg) decreased pro-inflammatory cytokine levels (IL-6, 14.6% and 18.5%; IL-1β, 23.1% and 32.6%), collagen content (27.7% and 50.1%), as well as matrix metalloproteinases-2, 9 (MMP-2, 9) expression (MMP-2, 11.8% and 18.5%; MMP-9, 16.2% and 21.1%). Sophocarpine (40 mg/kg) inhibited IκB-α phosphorylation (19.0%).Conclusion: These findings indicated that sophocarpine potentially had antifibrotic effects. The mechanism might be due to modulation of the balance between pro-inflammatory cytokine expression and collagen content level as well as MMPs expression via the NF-κB signaling pathway.

Anti-inflammatory effects of sophocarpine in LPS-induced RAW 264.7 cells via NF-κB and MAPKs signaling pathways

Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Our previous studies have showed that sophocarpine exerts anti-inflammatory activity in animal models. In the present study, anti-inflammatory mechanisms of sophocarpine were investigated in lipopolysaccharide (LPS)-induced responses in RAW 264.7 cells. Furthermore, the cytotoxicity of sophocarpine was tested. The results indicated that sophocarpine could increase the LDH level and inhibit cell viability up to 800μg/ml, and which was far higher than that of the plasma concentration of sophocarpine in clinical effective dosage. The results also demonstrated that sophocarpine (50 and 100μg/ml) suppressed LPS-stimulated NO production and pro-inflammatory cytokines secretion, including tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). These were associated with the decrease of the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, sophocarpine inhibited LPS-mediated nuclear factor-κB (NF-κB) activation via the prevention of inhibitor κB (IκB) phosphorylation. Sophocarpine had no effect on the LPS-induced phosphorylation of extracellular signal-regulated kinase 1/2 (Erk1/2), whereas it attenuated the phosphorylation of p38 mitogen-activated protein (MAP) kinase and c-Jun NH2-terminal kinase (JNK). Our data suggested that sophocarpine exerted anti-inflammatory activity in vitro, and it might attribute to the inhibition of iNOS and COX-2 expressions via down-regulation of the JNK and p38 MAP kinase signal pathways and inhibition of NF-κB activation.

Sophocarpine administration preserves myocardial function from ischemia-reperfusion in rats via NF-κB inactivation

Sophora alopecuroides L. (the clinical usefulness of compound Kudouzi injection) has been used mainly for the treatment of fever, inflammation, edema and pain. Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Sophocarpine injection (called the Kangke injection) has been demonstrated to have significant antivirus effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in clinical. The present study was to evaluate the protective effect of sophocarpine on the inhibition of NF-kappaB (NF-κB) and effect on inflammatory markers during myocardial ischemia-reperfusion (I/R) injury in rat. Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 2 h. 2 h after reperfusion was established, the hemodynamics and infarct size were examined. Blood samples were collected for biochemical analysis. Expression of NF-κB and mitogen-activated protein kinases (MAPKs) in ischemic myocardial tissue were assayed by western blot. Administration of sophocarpine significantly improved cardiac function and reduced infarct size in I/R rat heart in vivo. Furthermore, sophocarpine ameliorated the contents of inflammatory mediators (tumor necrosis factor-alpha, TNF-α; interleukin-6, IL-6; IL-10), neutrophil infiltration and myeloperoxidase (MPO) activity. Interestingly, sophocarpine also significantly inhibited translocation of NF-κB, which was associated with attenuated phosphorylations of p38 and c-Jun NH2-terminal protein kinase (JNK). Inflammatory mediators, infiltration of neutrophil, and MPO were ameliorated via down-regulation of JNK and p38, and inactivation of NF-κB. This might be one of the important mechanisms of sophocarpine that protected myocardial injury from I/R.

13C NMR spectroscopy of tri‐ and tetracyclic quinolizidine alkaloids. Compilation and discussion

A comprehensive collection of 13C chemical shifts of 159 tri- and tetracyclic quinolizidine alkaloids (sparteine derivatives) is presented. The data are discussed in terms of substituent effects, molecular geometries and protonation effects. Some IR, 1H and 15N NMR and MS data are included. © 1998 John Wiley & Sons, Ltd.

13 C NMR spectroscopy of tri‐ and tetracyclic quinolizidine alkaloids. Compilation and discussion

¹³ C NMR spectroscopy of tri‐ and tetracyclic quinolizidine alkaloids. Compilation and discussion

13C NMR spectroscopy of tri- and tetracyclic quinolizidine alkaloids. Compilation and discussion

13C NMR spectroscopy of tri- and tetracyclic quinolizidine alkaloids. Compilation and discussion

Superoxide anion scavenger properties of sparteine, a quinolizidine alkaloid from Lupinus

Summary Peroxidase activity in lupin ( Lupinus albus cv. Multolupa) hypocotyls is located, as are quinolizidine-type alkaloids, in epidermal tissues. Since these alkaloids have been shown to suffer a rapid turnover and degradation in lupin tissues, the ability of sparteine (a typical tetracyclic quinolizidine alkaloid) and cytisine (a typical tricyclic α-pyridone quinolizidine alkaloid) to act as peroxidase substrates was studied. However, neither alkaloid was oxidized by a partially purified lupin peroxidase fraction, or by horseradish peroxidase, as was ascertained by spectrophotometric and GC-MS studies. Likewise, these quinolizidine-type alkaloids were not substrates of a laccase of fungal origin. However, sparteine, unlike cytisine, acted as a superoxide scavenger, when the superoxide anions were generated in a phenazin methosulphate-NADH system and determined by the superoxide dismutase-sensitive reduction of nitroblue tetrazolium. The IC 50 value was 2.0 mmol/L. These results are discussed in the light of a possible protective role against oxidative damage of sparteine in Lupinus .

A novel O-tigloyltransferase for alkaloid biosynthesis in plants. Purification, characterization, and distribution in Lupinus plants.

A novel acyltransferase for alkaloid metabolism, tigloyl-CoA: (-)-13 alpha-hydroxymultiflorine/(+)-13 alpha-hydroxylupanine O-tigloyltransferase (HMT/HLTase), a monomeric 50-kDa protein, was purified to homogeneity from 10-day-old Lupinus termis seedlings. There were two isoforms of this acyltransferase with the same molecular mass (50 kDa) but slightly different isoelectric points (pI 7.8 and 7.6). These two isoforms showed the same catalytic activity of tigloyl transfer from tigloyl-CoA to (-)-13 alpha-hydroxymultiflorine and (+)-13 alpha-hydroxylupanine, which belong to the same (7S, 9S) enantiomeric series of tetracyclic quinolizidine alkaloids; whereas no activity was detected toward an antipodal (7R, 9R) alkaloid, (-)-baptifoline, or to bicyclic quinolizidine alkaloids, (+)-epilupinine and (-)-lupinine. The Km values for HMTase activity were determined to be 21 microM and 46 microM for (-)-13 alpha-hydroxymultiflorine and tigloyl-CoA, respectively; and for HLTase activity, 27 microM and 52 microM for (+)-13 alpha-hydroxylupanine and tigloyl-CoA, respectively. The activity was inhibited by CoASH in a competitive manner, and by (+)-lupanine and (+)-epilupinine in a partially noncompetitive manner. The enzyme showed the highest activity around pH 8.0 and was inactivated by heat treatment and by the addition of sulfhydryl blocking reagents. Such tigloyltransferases for quinolizidine alkaloid metabolism are distributed in some Lupinus species and Cytisus scoparius, in which tigloyl alkaloids are accumulated in addition to non-ester-type alkaloids, but not in other lupin plants, in which only non-ester-type alkaloids are present.

Distribution and taxonomic significance of major alkaloids in the genus Podalyria

A chemotaxonomic survey of alkaloids in 22 species of the genus Podalyria has shown the presence of several different tetracyclic quinolizidine alkaloids and their angelate, tigliate and carboxylic acid esters. Quantitative and qualitative differences were found between the species and also between samples of twigs, leaves, pods and seeds. Most of the species have high concentrations of lupanine as virtually the only alkaloid, but some have a wide range of different compounds, including various hydroxylated lupanines and esters of alkaloids. The three yellow-flowered species differ from all others in the presence of virgiline, oroboidine and virgiline-pyrrolyl carboxylic acid ester as major alkaloids. These three compounds were found to be totally absent in all the pink- and white-flowered species of the genus. In the tribe Podalyrieae, carboxylic acid esters were hitherto known only from the genus Virgilia and their distribution agrees with morphological evidence that the yellow-flowered group of species should be excluded from Podalyria.

Taxonomic significance of major alkaloids in the genus Priestleya

The genus Priestleya is known to contain the bipiperidyl alkaloid anabasine and an alkaloid tentatively identified as lupanine. In a study of 16 different species, several quinolizidine alkaloids and some bipiperidyl alkaloids were identified. A remarkable difference was found between the two sections of Priestleya: sect. Priestleya contains sparteine, lupanine and other tetracyclic quinolizidine alkaloids, while the sect. Anisothea contains the bipiperidyl alkaloid anabasine and the bicyclic quinolizidine lupinine. The chemical distinction agrees with morphological evidence that the generic concept of Priestleya is artificial and that two distinct genera should be recognized.

Alkaloids of Virgilia divaricata and V. oroboides

orty-three quinolizidine alkaloids, and the dipiperidyl alkaloid, ammodendrine, have been found in Virgilia divaricata and V. oroboides. Three new quinolizidine alkaloids were detected, viz. virgilidone, 4β- O-(2′-pyrrolylcarboxyl)- epilupinine and 4β-hydroxy-1 1- O-(2′-pyrrolylcarboxyl)-epilupinine. The distribution of alkaloids in air-dried leaves, flowers, pods, seeds and twigs of the two species was also investigated. The unique combination of bi-, tri- and tetracyclic quinolizidine alkaloids is typical of the genus Virgilia.