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Bladder and Prostate Cancer
Published in Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri, Plants That Fight Cancer, 2019
Charlie Khoo, Yiannis Philippou, Marios Hadjipavlou, Abhay Rane
An English language literature search was performed on Ovid Embase, Ovid Medline, Scopus, and Web of Science to identify studies investigating the potential chemotherapeutic role of various plants and plant extracts against prostate, bladder, and renal cancers. The focus was on agents that have undergone extensive research directed towards understanding their chemotherapeutic mechanisms and on which clinical trials have been undertaken (although a few promising agents with in vitro trials have been included). Furthermore, we concentrated primarily on clinical data that relates to treatment rather than prevention of cancer. Search terms included ‘prostate cancer’, ‘bladder cancer’, ‘plant extract’, ‘selenium’, ‘vitamin E’, ‘pomegranate’, ‘green tea’, ‘curcumin’, ‘resveratrol’, ‘silibinin’, ‘gingko’, ‘modified citrus pectin’, ‘phellodendron amurense’, ‘red clover’, ‘Salvia’ and ‘mistletoe’, ‘PC-SPES’, ‘Zyflamend’, and ‘Profluss’.
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
The monocytic MDSCs, dubbed Mo-MDSCs, found in psoriasis are reported to produce more IL23, IL1β, and CCL4 cytokines than Mo-MDSCs from healthy controls, and are dysfunctional on their suppressive action on T cells. Circulating MDSC levels are significantly increased in psoriasis than in healthy controls. These cells are also capable of producing MMP9, MMP1, IL8, GROα, and modified citrus pectin (MCP) 1, thus contributing to inflammation and angiogenesis.
An updated patent review of galectin-1 and galectin-3 inhibitors and their potential therapeutic applications (2016–present)
Published in Expert Opinion on Therapeutic Patents, 2021
Aaftaab Sethi, Swetha Sanam, Ravi Alvala, Mallika Alvala
Various strategies have been reported to target galectins. Galectin inhibitors can be divided into two groups: Carbohydrate based galectin inhibitors and non-carbohydrate-based galectin inhibitors. Carbohydrate-based inhibitors include glycodendrimers and modified saccharides like galactose-based, talose-based, lactose-based, N-Acetyllactosamine-based and thiodigalactoside-based inhibitors [47]. Modified Citrus Pectin (MCP, PectaSol-C) and Davanat (GM-CT-01) are the natural polysaccharides with putative galectin inhibitory activity [48,49]. Non-carbohydrate-based inhibitors include peptide-based inhibitors, peptidomimetics and heterocyclic compounds [5]. Anginex (β-pep25) is a synthetic peptide that inhibits gal-1 and exhibits antiangiogenic and anti-tumor effects [50]. DiBenzoFulvene (DBF) is a partial peptidomimetic and its derivative 6DB7 is a gal-1 inhibitor with angiostatic activity [51]. OTX008 (PTX008/Calixarene 0118) is an allosteric inhibitor of gal-1 which has anti-tumor and anti-angiogenic activity [52,53]. Some heterocyclic molecules with galectin inhibitory activity have also been reported [54–61]. Few allosteric inhibitors of galectins, i.e., molecules that bind outside of its carbohydrate-binding site are reported. These include 6DBF7 (gal-1 inhibitor), OTX008 (gal-1 inhibitor) and analogues of tetrahydroisoquinoline natural products (gal-3 inhibitors) [51,53,62].
Ultrasonic Modified Sweet Potato Pectin Induces Apoptosis like Cell Death in Colon Cancer (HT-29) Cell Line
Published in Nutrition and Cancer, 2018
Fredrick Onyango Ogutu, Tai-Hua Mu, Hongnan Sun, Miao Zhang
Modified citrus pectin (MCP) is currently used in prostate cancer therapy with laudable success. It increases the doubling time of prostate-specific antigen in men with prostate cancer (16). The use of modified pectins in cancer research has mainly focused on acid, enzymatic, and heat-modified pectins. However, sonication may have potential owing to it being cheap, rapid, easy to upscale and efficient with no post treatment cleaning steps (17). Recent research on ultrasonic-modified sweet potato pectin showed that it led to increased antioxidant activity (18). Hence, the current study assessed the anticancer activity of ultrasonic-modified sweet potato pectin against colon cancer cell line (HT-29).
Latifolin protects against myocardial infarction by alleviating myocardial inflammatory via the HIF-1α/NF-κB/IL-6 pathway
Published in Pharmaceutical Biology, 2020
Xiao-Xiao Lai, Ni Zhang, Lan-Ying Chen, Ying-Ying Luo, Bin-Yao Shou, Xin-Xu Xie, Rong-Hua Liu
In the initial stage of MI (the inflammatory phase), large amounts of neutrophils and monocytes/macrophages infiltrate into the myocardium (Weirather et al. 2014), causing increased release of inflammatory factors to resolve the harsh inflammatory environment, which further aggravates myocardial injury. In the later stage of MI (the proliferation phase), chronic inflammation is mainly regulated by macrophages (Lambert et al. 2008). When the intense inflammatory phase has subsided, macrophages secrete chemokines to recruit and activate fibroblasts and endothelial cells. Transforming growth factor-β (TGF-β) is one of the important factors for macrophage release. It is involved in the transformation of fibroblasts into myofibroblasts, which in turn the vast production and deposition of extracellular matrix proteins for scar formation (Serini et al. 1998). In the last phase of MI (the maturation phase), the infarct evolves into a mature scar with cross-linked collagen fibres leads to the myocardial infarct area continues to expand, which further aggravate the progression of myocardial fibrosis and poor ventricular remodelling. As inflammatory response plays an important role in all stages of the development of MI, an increasing number of studies consider anti-inflammatory as a strategy for the treatment of MI. Xu et al. (2020) demonstrated that the Gal-3 inhibitor modified citrus pectin ameliorated cardiac dysfunction, decreased myocardial injury and reduced collagen deposition through inhibiting inflammation. Liu et al. (2019) found that fisetin treatment improved cardiac function, inhibited macrophage recruitment into the left atrium and production of interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α), and attenuated adverse atrial fibrosis following acute myocardial infarction.