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Pharmacological actions of chemical constituents
Published in C. P. Khare, Evidence-based Ayurveda, 2019
In accordance with structural forms, the alkaloids are classified in diterpenoid alkaloids (14-O-acetylneoline, 14-O-veratroylpseudaconine, and hypaconitine), indole alkaloids (fumigaclavine C and isatin), indolonaphthyridine alkaloids (nigakinone), indoloquinazoline alkaloids (tryptanthin), isoquinoline alkaloids (berberine, boldine, cavidine, coptisine derivatives, EM012, papaverine, sanguinarine, sinomenine, tetrahydrocoptisine, and tetrandrine), phenanthroindolizidine alkaloids (NK-007 and W-8), piperidine alkaloids (piperine), purine alkaloids (caffeine), quinoline alkaloids (skimmianine) and quinolizidine alkaloids (matrine, oxymatrine, sophocarpine, and sophoridine).
Phytoextracts and Their Derivatives Affecting Neurotransmission Relevant to Alzheimer’s Disease
Published in Akula Ramakrishna, Victoria V. Roshchina, Neurotransmitters in Plants, 2018
Quinolizidine alkaloid: Huperzine A:Huperzine A [Figure 21.3 (xiii)], isolated from the clubmoss Lycopodium serratum (Family: Lycopodiaceae), showed AChE inhibitory activity in vivo. α-Onocerin [Figure 21.3 (xiv)] a triterpene-type compound, from L. clavatum also showed 50% activity against AChE (Orhan et al., 2003). Huperzine A is also a NMDA receptor antagonist, which protects the brain against glutamate-induced damage, and it increases nerve growth factor levels (Eduardo et al., 2012).
Protecting Pancreatic β-cells from Metabolic Insults
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Evidence is available to demonstrate that quinolizidine alkaloids from members of the genus Lupinus L. decrease glycemia by promoting insulin secretion. Sparteine administered intravenously at a single bolus of 15 mg/kg and 90 mg over 60 minutes in type 2 diabetic patients evoked a decreased of glycemia and increase of plasma insulin.184 Multiflorine (Figure 2.9), isolated from Lupinus albus L. given intraperitoneally at a dose of 30 mg/kg halved the postprandial 60 minutes peak glycemia of ICR mice subjected to oral glucose tolerance test.185 Sparteine and thionosparteine at a dose of 8.6 mg/kg and lupanine at a dose of 22.1 mg/kg given intraperitoneally to rodents poisoned with streptozotocin lowered glycemia at 90 minutes as potently as glibenclamide given orally at a dose of 3 mg/kg.186 Furthermore, 2-thionospareine, lupanine, 13-α-hydrohylupanine or 17-oxo-lupanine at a dose of 0.5 mM enhanced the secretion of insulin by isolated pancreatic islets challenged with glucose in vitro and this effect was inhibited by the opener of KATP-sensitive channels diazoxide.187 Total alkaloids extract of seeds of from Lupinus mutabilis Sweet given at a dose or at a dose of 2.5 mg/kg to type 2 diabetic subjects on low dose of metformin evoked after 90 minutes a 9.9% decrease in glycemia.188 Lupanin (Figure 2.10) which given orally at a single dose of 20 mg/kg to streptozotocin-induced diabetic Wistar rats 30 minutes before oral glucose lowered postprandial glycemia at 60 minustes.189 In healthy rats, oral administration of lupanin had no effect.189 Lupanin at a concentration of 0.5 mmol/L enhanced the secretion of insulin by rat islets exposed to high (15 mmol/L) but not low (8 mmol/L) glucose by about 140%.189 This quinolizidine alkaloid inhibited KATP current, increased the frequency of calcium action potential. Insulin secretion by lupanine was increased by coadministration of arginine.189 In human pancreatic α-cells secrete acetylcholine as paracrine transmitter when plasma glucose is low to sensitize β-cells to forthcoming increase in glycemia.190 In rodents, acetylcholine is released from parasympathetic nerves and β-cell express muscarinic receptor M1, the activation of which induces insulin secretion.128 While glucose is the primary stimulus for insulin secretion, neurotransmitters and hormones bind to specific cell surface receptors.73 Vagal activation releases acetylcholine which binds to M3 muscarinic receptors, activate phospholipase C via G protein-coupled mechanism, stimulating phosphoinositide hydrolysis to release diacylglycerol and inositol 3-sphosphate resulting in insulin secretion.191 Quinolizidines have affinities for muscarinic receptors.192 Deciphering the precise insulinotropic and, if any, cytoprotective pathways involved in Lupinus alkaloids may participate in the development of new leads for metabolic syndrome and associated type 2 diabetes. Furthermore, studies on the beneficial effect of Lupinus albus L. seeds consumptions in metabolic syndrome are needed.
Aloperine protects human retinal pigment epithelial cells against hydrogen peroxide–induced oxidative stress and apoptosis through activation of Nrf2/HO-1 pathway
Published in Journal of Receptors and Signal Transduction, 2022
Junhui Zhang, Haitao Zhou, Juanli Chen, Xiaoyan Lv, Hongsong Liu
Aloperine is a quinolizidine alkaloid that has displayed multiple pharmacological functions in several chronic diseases through its anti-oxidative activity. Aloperine ameliorates oxidative stress patterns in mouse Neuro2a (N2a) cells by reducing the production of ROS and 4-hydroxy-2-nonenal (4-HNE). Aloperine also inhibits the apoptosis of N2a cells via a mitochondria-dependent pathway [15]. Aloperine attenuates expressions of inflammatory mediators, enhances SOD expression to increase ROS detoxification, and promotes the expression of anti-apoptotic bcl-2, thereby preventing tubular cells from ischemia-reperfusion (IR)-induced cell injury [21]. Aloperine alleviates allodynia and hyperalgesia induced by neuropathic pain due to anti-oxidative activity with increased T-AOC, GSH-PX and T-SOD concentration, and reduced MDA concentration [22]. In addition, aloperine was found to attenuate H2O2-induced nucleus pulposus cells via elevating the activities of SOD and GSH-PX, inhibiting cell apoptosis and suppressing the NF-κB signaling pathway [23]. Therefore, we speculated that aloperine might have protective effect on H2O2-induced ARPE-19 cells. Our results demonstrated that aloperine improved cell viability, and attenuated H2O2-induced oxidative stress and apoptosis in ARPE-19 cells. These findings suggested that aloperine protected ARPE-19 cells from H2O2-induced oxidative damage, implying aloperine might be a therapeutic agent for the treatment of AMD.
Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2020
Wan-Ting Xu, Tian-Zhu Li, Shu-Mei Li, Cheng Wang, Hao Wang, Ying-Hua Luo, Xian-Ji Piao, Jia-Ru Wang, Yu Zhang, Tong Zhang, Hui Xue, Long-Kui Cao, Cheng-Hao Jin
Apoptosis, one of the strategies for cancer treatment, involves activation of a series of molecular events and is induced via various extracellular stresses including reactive oxygen species (ROS). A relatively high level of ROS induces redox imbalance, causing cell apoptosis during the physiological and pathological progression of cancer [6]. Tumour cells with higher ROS levels are more likely to be killed than normal cells with lower ROS levels, as elevated levels of ROS can activate multiple signalling pathways that induce apoptosis such as mitogen-activated protein kinase (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor-kappa B (NF-κB) signalling pathways [7]. Accordingly, targeting relevant signalling pathways, especially ROS-related pathways, may have potential for lung cancer treatment [8]. Some quinolizidine alkaloids have been reported to exert pro-oxidant actions, which may be an important mechanism for their anticancer and apoptosis-inducing properties [9].
Matrine protects PC12 cells from lipopolysaccharide-evoked inflammatory injury via upregulation of miR-9
Published in Pharmaceutical Biology, 2020
Matrine has long been known as an anti-inflammatory quinolizidine alkaloid (Kan et al. 2013). For instance, matrine was able to repress LPS-induced inflammation in intestinal cells (Wu et al. 2017) and lung epithelial cells (Liou et al. 2016). The similar function of matrine was observed in this study in LPS-damaged PC12 cells, as evidenced by the repressed release of pro-inflammatory cytokines, including IL-1β, IL-6 and TNF-α. Besides, the anti-apoptotic activity of matrine in various experimental systems was previously revealed, such as hypoxia/reoxygenation-injured cardiac microvascular endothelial cells (Zhao XB et al. 2018) and focal cerebral ischaemic mice (Zhao et al. 2015). In line with this, matrine also exerted anti-apoptotic property in LPS-damaged PC12 cells. And matrine prevented PC12 cells from initiating apoptosis possibly via a mitochondrial-dependent pathway, since the balance of Bcl-2 and Bax was disturbed. Altogether, the findings of this paper evidenced the neuroprotective property of matrine, which was consistence with findings reported elsewhere (Meng et al. 2017).