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Anti-Inflammatory Properties of Bioactive Compounds from Medicinal Plants
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Muhammad Imran, Abdur Rauf, Anees Ahmed Khalil, Saud Bawazeer, Seema Patel, Zafar Ali Shah
In LPS-stimulated microglia, β-LAP (β-lapachone) from lapacho tree suppressed the iNOS expression, pro-inflammatory cytokines and MMPs (MMP-3, -8, and -9) at protein and mRNA levels. In contrast, β-LAP elevated the expressions of HO-1, IL-10, and TIMP-2 (tissue inhibitor of metalloproteinase-2). In an LPS-activated systemic inflammatory mouse model, anti-inflammatory potential associated with β-LAP was validated. In the LPS-treated mouse brain, β-LAP retarded activation of microglial and iNOS expressions, MMPs, and pro-inflammatory cytokines levels. Additionally, in LPS-activated microglia, studies regarding mode of action of β-LAP revealed anti-inflammatory potential by retarding NF-κB/AP-1, MAPKs, and PI3K/AKT signaling pathways. The β-LAP aided in suppressing the production of ROS by inhibiting phosphorylation of NADPH oxidase subunit proteins. Antioxidative properties of β-LAP seemed to increase NAD(P)H:quinone oxidoreductase-1 (NQO1) and HO-1 through Nrf2/ARE and PKA-pathways [74]. In mice (C57BL/6), β-LAP decreased, the instant hypersensitive response tempted by Con A (concanavalin A). Therefore, Th2 inhibited IL-10, IL-4, IL-6, and IL-5 averting the incidence of various allergic-inflammations and allergies [2].
Medication: Nanoparticles for Imaging and Drug Delivery
Published in Harry F. Tibbals, Medical Nanotechnology and Nanomedicine, 2017
Another example of a natural product-derived drug that can be enhanced by nanoparticle delivery is the promising compound β-lapachone, an o-naphthoquinone found in the bark of the South American lapacho tree. β-lapachone is known to induce cytotoxic effects in a wide variety of malignant human cell types including colon, lung, prostate, breast, pancreatic, ovarian, and bone cancers, as well as some blood cancers and retinoblastoma [384].
Catalog of Herbs
Published in James A. Duke, Handbook of Medicinal Herbs, 2018
According to Hager’s Handbook,33 the wood of T. ipe contains circa 3.7% lapachol (C15H14O3); the essential oil ranges from 0.55 to 1.49% (predominantly sesquiterpenes), resin 3.3 to 4.5%, waxy matter with ceryl alcohol and lignoceric acid 0.95 to 1.18%, lactone bitter substances 0.85 to 1.4%, glycosidol bitter substances 0.025 to 0.042%, 12.2 to 17.8% tannin, yielding protocatechuic acid, and 3 to 4% acids and neutral saponins; wood also contains napthaquinones and anthraquinones. The latter might explain its folk usages for psoriasis. According to Prakash and Singh,309 the stembark of T. pentaphylla contains lapachol, nonacosane, dehydrotectol, and beta-sitosterol, the roots hexacosane, dehydrotec-tol, beta-sitosterol, and oleanolic acid. Some species contain xyloidone, which is active against Brucella and Candida. Much of the activity may be traced to the lapachol. Lapachol has shown antimalarial activity in animals.309 It is known to uncouple oxidative phosphorylation. Lapachol, active against Gram-positive and acid-fast bacteria, as well as fungi, was once of great interest to the NCI. Lapachol was found to have anticancer activity. Filed in 1967, lapachol was dropped from NCI investigations because of therapeutic inactivity. Reported by Hartwell4 from Stereospermum suaveolens, lapachol occurs in several species of Tabebuia, e.g., T. rufescens and T. serratifolia. Old correspondence from Hartwell suggests that lapachol has also been isolated from woods of taigu, greenheart, lapacho, mao, ipedo campo, ipeamarillo, ipe tabaco, mostly species of Bignonia, Tabebuia, and Tecoma. In my “Phytotoxin Tables”,151 cited Avicennia, Bassia, Bignonia, Paratecoma, Tabebuia, Tecoma, and Tectona with questionable citations for Adenanthera, Andira, and Intsia. Brazilian species of Tabebuia, known as pao d’arco and lapacho, have gotten big press sporadically over the last 50 years as cancer remedies. Thus, Stereospermum and Tabebuia, classical sources of lapachol, both have folk histories as “cancer remedies”. I have received unsolicited testimonials from “recovered patients” supposedly cured by pao d’arco. Recently, I submitted an unvouchered sample of ipe roxo (“Tecoma curialis”) to the NCI for screening. This is also labeled pao d’arco herbal tea. There are no cancer claims on the label, but the pao d’arco has gotten enough press to generate a North American interest in lapachol, dropped by NCI because of “no therapeutic effect.” Hartwell4 notes that lapachol was carried into clinical trial because “of its high Walker 256 activity even when given orally.” Lack of toxicity permitted large oral doses but sufficiently high blood levels could not be obtained to show a therapeutic effect. While lapachol was inactive against LI210 leukemia, the sodium salt of lapachol was active.
Development of solid dispersions of β-lapachone in PEG and PVP by solvent evaporation method
Published in Drug Development and Industrial Pharmacy, 2018
Klecia M. dos Santos, Raquel de Melo Barbosa, Fernanda Grace A. Vargas, Eduardo Pereira de Azevedo, Antônio Cláudio da Silva Lins, Celso A. Camara, Cícero F. S. Aragão, Tulio Flavio de Lima e Moura, Fernanda Nervo Raffin
βlap (3,4-dihydro-2,2-dimethyl-2 H-naphthol[1,2-b]pyran-5,6-dione) was supplied by Laboratório de Síntese de Compostos Bioativos (UFRPE, Brazil). βlap was obtained by acid cyclization of lapachol, which was extracted from the bark of the lapacho tree (Tabebuia avellanedae). PEG (6000), PVP (K30), and absolute ethanol were obtained from Synth (São Paulo, Brazil). Sodium lauryl sulfate (SLS) was purchased from Sigma-Aldrich (St Louis, MO, USA). All other materials were of analytical grade.
A pH/ROS cascade-responsive and self-accelerating drug release nanosystem for the targeted treatment of multi-drug-resistant colon cancer
Published in Drug Delivery, 2020
Na Chang, Yufei Zhao, Ning Ge, Liting Qian
Insufficient release of nanomedicines in cells can also lead to the failure to attain effective intracellular therapeutic concentrations of a drug (Tang et al., 2017; Wang et al., 2018). Hence, controlled drug release at target sites in response to intracellular stimuli such as ROS, enzyme activity, pH, or glutathione (GSH) may be required to achieve sufficient drug levels and overcome MDR (Zhu et al., 2017; Raza et al., 2019). Consequently, enzyme-responsive nanomedicines have received increasing attention, particularly those that involve NAD(P)H quinone dehydrogenase 1 (NQO1), an enzyme that specifically reduces quinones to hydroquinone through catalytic two-electron reduction (Vasiliou et al., 2006). NQO1 is overexpressed in numerous solid tumors, such as breast, colon, and lung cancers, by up to 100-fold (Ye et al., 2017). Beta-lapachone (Lapa), a substrate of NQO1, is extracted from the bark of the lapacho tree (Siegel et al., 2012; Wang et al., 2019). Lapa is reduced to an unstable hydroquinone through the activity of NQO1, and is rapidly oxidized back to the parent quinone in the presence of molecular oxygen (Siegel et al., 2012; Wang et al., 2019). This redox cycling can generate high concentrations of ROS, and, because the NQO1 enzyme is not involved in the oxidation reaction, ROS is continuously generated to trigger drug release (Li et al., 2019). This suggests that co-delivery of Lapa with a ROS-responsive nanomedicine may specifically increase the level of ROS stimulus in cancer cells and surround tumor tissue with a heterogeneous distribution of ROS. This would lead to a cascade amplification, which would accelerate the release of the drug and eventually overcome the insufficient levels of intracellular drug release. Moreover, Lapa-induced ROS production is accompanied by NAD(P)H/ATP consumption, which can affect the activity of P-gp-associated factors such as HIF-1α, NF-κB, and caspase, ultimately leading to the downregulation of P-gp (Choi et al., 2003; Woo et al., 2006). Therefore, Lapa can effectively reverse MDR through ATP consumption and modulation of P-gp.