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Natural Product Compounds from Plants in Neurodegenerative Diseases
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Priya Darshani, Md TanjimAlam, Prem P. Tripathi, V.S. Pragadheesh
Vinpocetine, a semi-synthetic chemical derived from the vincamine, present in the leaves of Vinca minor L., is used for the treatment of dementia and mental impairment. Vinpocetine is sold as a drug in Europe named Cavinton, whereas, in the United States, it is sold as a dietary supplement to treat memory loss. Vinpocetine has been reported to enhance neurotransmitter production in the brain and improve cerebral metabolism by enhancing the glucose and oxygen consumption in the brain and elevating cerebral cAMP and ATP levels. It has been shown to ameliorate microcirculation and cerebral blood flow by inhibiting platelet aggregation. Vinpocetine has been evaluated in several double-blind clinical trials that demonstrated its significant benefits in patients of AD (Szatmari and Whitehouse, 2003; Balestreri et al., 1987).
Antitubulin Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The two well-known Vinca alkaloids, vinblastine and vincristine (Figure 4.7), are minor constituents of the Madagascar periwinkle (Vinca rosea) (Figure 4.6). The periwinkle is the common name for herbs of the dogbane family, which make up the genus Vinca of the family Apocynaceae. The lesser periwinkle, a native of many parts of Europe, grows in woods and thickets and is classified as Vinca minor. The greater periwinkle, which has much larger flowers and ovate- to heart-shaped leaves, is a native of southern Europe and is classified as Vinca major. The periwinkle contains numerous other alkaloids in addition to vinblastine and vincristine.
Inhibiting Low-Density Lipoproteins Intimal Deposition and Preserving Nitric Oxide Function in the Vascular System
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Vinpocetine is a synthetic derivative of vincamine isolated from Vinca minor L.290 FVB/NJ mice with ligated left carotid artery intraperitoneally injected with 5 mg/kg vinpocetine daily for 14 days had reduced vascular smooth muscle cell proliferation. This indole alkaloid increased luminal area and prevented thrombosis and intraplaque haemorrhage.291 This alkaloid at a concentration of 100 µM reduced the wall thickness developed by human saphenous vein cultured ex vivo for 7 days.291In vitro, vinpocetine at 70 µM inhibited the proliferation of smooth muscle cells via cell cycle inhibition via downregulation of cyclin D1 and upregulation of p27Kip1.291 This alkaloid inhibited the migration of vascular smooth muscle cells induced by platelet-derived growth factor at 50 µM, and inhibited collagen synthesis. It limited platelet-derived growth factor-induced reactive oxygen species production, and consequently activated extracellular signal-regulated kinase-1/2.291 This molecule could be of value in Metabolic Syndrome.
Effect of different doses of borneol on the pharmacokinetics of vinpocetine in rat plasma and brain after intraocular administration
Published in Xenobiotica, 2020
Qun Ma, Manman Dai, Huimin Zhang, Luyu Bai, Ning He
Vinpocetine (VIN), a vincamine derivative, is an extract from the Vinca minor plant and was the first identified nootropic. Vinpocetine exerts several pharmacological and biochemical effects, including neuroprotection effects, the promotion of brain metabolism, and the improvement of brain microcirculation. VIN was first marketed in Hungary, and is mainly administered orally and intravenously for the treatment of ischemic stroke and other cerebrovascular diseases, such as residual cerebral hemorrhage, residual cerebral infarction, and cerebral artery cirrhosis (Bereczki & Fekete, 1999; Lin et al.,2014). However, a previous study clearly showed that its low water solubility (∼5 µg/mL), poor absorption, and first-pass effects resulted in very low oral bioavailability (∼7%) of VIN in humans, which may limit its clinical application (Grandt et al., 1989). Furthermore, VIN has a short elimination half-life (1–2 h) following intravenous administration, resulting in the need to administer frequent doses (three times daily), extensive distribution in the body, and higher drug concentrations in the lung, spleen, liver, and kidney than in the brain (Zhuang et al., 2010). An alternative route of administration may help to overcome these problems.
IgG antibodies mediated gold nanoparticles conjugated to methotrexate as targeted chemotherapy for lung cancer
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Asad Syed, Abu Baker, Mohamed Mohany, Abdallah M. Elgorban, Mohd Sajid Khan, Salim S. Al-Rejaie
IgG, the most preferably used antibody [27], targets and acts against cancer via complement activation (by inserting the lytic membrane attack complex in the tumour cell membrane or initiating NK/macrophages), inhibition of critical intracellular signal transduction pathway(s), or antibody-dependent toxicity. The unaltered 3D structure of IgG antibodies on IgGAuGNPs was found to recognise and annihilate lung cancer cells via Fcγ receptors [27,28]. The role of the most abundant antibody, IgG, in current antibody drugs is predominant due to their promising potency, better pharmacokinetics, pharmacodynamics, long half-life, and restricted off-target toxicity. However, there are limitations to their use against cancer. Limitations such as poor penetration and bystander activation of the immune system can be overcome using nanoparticles. Therefore, bioconjugation of IgG with NPs enhances their role against cancer. An intact, highly polar IgG antibody spans enough time in the blood to reach its target because the liver clears it, whereas smaller antibodies (<60 kDa) are cleared by the kidneys [29]. Vincamine, an alkaloid with distinct pharmaceutical activities, is a natural product of Vinca minor leaves [30]. Vincamine, a powerful antioxidant, neuroprotective, and anti-tumour agent, works against ischaemia and hypoxia by generating ATP via oxygen and glucose [31]. It is also known to carry oxygen in living cells [32]. It is recommended as a dietary supplement (40–80 mg/d for 20–40 d without noticeable side effects) to stimulate the CNS and enhance memory [32]. It downregulates the NF-κB-mediated iNOS expression after upregulating the Nrf2/HO-1 mediated signalling pathway(s) that eventually regulate the expression of antioxidant genes like SOD, CAT, and HO-1 [33]. Vincamine also depletes the intracellular iron concentration (and hence dysregulates IRP-2) [34] and disrupts mitochondrial membrane potential for directly activating caspase-3 [35]. Nanoparticles and hydrophilic moieties of vincamine and IgG antibodies can avoid recognition by the reticuloendothelial system (RES). Their accumulation in solid tumours is enhanced by the permeation and retention (EPR) effect with prolonged circulation time in the bloodstream. The bioconjugation of drugs with NPs also prevents non-specific interactions.