Gingers and Their Purified Components as Cancer Chemopreventative Agents

Abstract

Chemoprevention by ingested substituents is the process through which nutraceuticals and/or their bioactive components antagonize carcinogenesis. Carcinogenesis is the course of action whereby a normal cell is transformed into a neoplastic cell. This latter action involves several steps, starting with initiation and followed by promotion and progression. Driving these stages is continued oxidative stress and inflammation, which in turn, causes a myriad of aberrant gene expressions and mutations within the transforming cell population and abnormal gene expressions by the cells within the surrounding lesion. Chemoprevention of cancer with bioreactive foods or their extracted/purified components occurs primarily via normalizing these inappropriate gene activities. Various foods/agents have been shown to affect different gene expressions. In this review, we discuss how the chemoprevention activities of gingers antagonize cancer development.

Mechanisms of Chemopreventive and Therapeutic Proprieties of Ginger Extracts in Cancer

“…On the other hand, angiogenesis is a crucial event for tumor progression and metastatic cascade, therefore many cancer therapies are directed against the tumor-associated vasculature [ 69 , 70 , 71 ]. Recent observation showed that a series of natural compounds, including ginger extracts, were proposed as antiangiogenic/angiopreventive substances both in in vitro and in vivo [ 20 , 26 ]. In this contest, it was demonstrated that 6-gingerol was able to inhibit the proliferation and tube formation of human umbilical vein endothelial cells (HUVECs) in response to VEGF or bFGF [ 9 ].…”

“…Furthermore, they inhibit angiogenesis, CSCs formation, and the EMT process. Therefore, this natural compound directly and indirectly influences tumor cell survival and inhibits invasion and metastasis processes, without significant toxic effects on normal cells [ 18 , 26 ]. Additionally, ginger enhances the therapeutic efficacy of the currently available anti-cancer drugs and represents a good adjuvant to certain phytochemical compounds including turmeric, garlic, and gelam honey [ 103 , 104 ].…”

Chondroprotection and Molecular Mechanism of Action of Phytonutraceuticals on Osteoarthritis

“…ADAMTS is the primary OA prevention and treatment method since the overactive catabolic activity of MMPs causes cartilage degradation. Epigallocatechin-3-gallate inhibits expression of ADAMTS-1, -4 and -5 in chondrocytes, the activity of proteolytic enzymes in joint tissues, including synoviocytes and tendons, TNF-α-induced production of MMP-1 and MMP-3, IL-1β-induced expression of MMP-1, -3, and -13 in human tendon fibroblasts [ 114 , 115 , 116 , 117 ]. In vitro studies have confirmed an increase in the anticatabolic potential and activity of tissue inhibitors of MMP (TIMP) -1 and -2 under the action of epigallocatechin-3-gallate [ 95 , 118 ].…”

“…The natural polyamine spermidine has a cardioprotective effect, dietary spermidine can reduce TNF-α in plasma [ 117 ] and further increase the bioavailability of NO by reducing oxidative stress in cardiomyocytes [ 120 ]. In another study, intraperitoneal injection (IP) of a spermidine analog, spermine, decreased TNF-α in the plasma of septic mice by inhibiting high motility group protein-1 and the release of inflammatory cytokines in macrophages [ 121 ].…”

The activity of bioactive compounds against several diseases by modulating autophagy

“…According to the latest research, GIN has anti-cancer properties, such as 6-gingerol reduces tumor volume and weight in A549 lung carcinoma cells by increased the accumulation of ROS and iron resulting in cell death (Tsai et al, 2020). Potential activity of 6gingerol also was found in cervix cancer by inducing apoptosis protein agents, such as caspase 3 and 6 (Lechner and Stoner, 2019;Ho et al, 2013) and PRPP; the ratio of Bax/Bcl-2; as well as reactivation of p53 (Zhang et al, 2017a), (Rastogi et al, 2015). Another bioactive compound of gingerol, 10-gingerol, was found to induce apoptosis in breast cancer by targeting mitochondrial membrane permeabilization (MMP), and caspase-independent apoptosis (CIA) by its analog SSi6 (Luna-Dulcey et al, 2018; Bernard et al, 2017).…”