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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
Ginsenoside, a saponin, is the most potent phytochemical used for the treatment of ALS. It reduces iNOS and COX-2 expression levels in LPS-induced BV-2 cells, indicating its effective role in inhibiting the M1 polarization of microglia (Jin et al., 2019). Apart from these, phytoconstituents like madecassoside, epigallocatechin gallate, diallyl trisulfide, ampelopsin, morroniside, picroside-II and astragaloside IV have been reported by researchers for their beneficial activity against oxidative stress in different ALS animal models (Zhang et al., 2013).
Rhubarb
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Ethnopharmacology of Wild Plants, 2021
Gan B. Bajracharya, Richa K. Gupta
Stilbenes ε-viniferin (104) and ampelopsin B (105) showed a remarkable inhibitory effect on lipoxygenase and exhibited strong free radical scavenging activity against ABTS•+ radical cation (Ngoc et al. 2008).
3,3′-Diindolylmethane enhances apoptosis in docetaxel-treated breast cancer cells by generation of reactive oxygen species
Published in Pharmaceutical Biology, 2018
Susan Lanza-Jacoby, Guanjun Cheng
NOX2 is expressed in breast cancer cells (Satooka and Hara-Chikuma 2016). However, the role of NOX2 in mediating the effects of the chemotherapeutic drugs in breast cancer has not been explored. This is the first study to show that DIM in combination with DOC increased NOX2 expression along with elevating ROS, while the individual compounds had no effect. A recent study demonstrated that the combination of erlotinib with ampelopsin induced apoptosis and increased ROS production through the up-regulation of NOX2 (Hong et al. 2017). Further studies are needed to investigate the role of NOX2 in ROS production in breast cancer. Inhibiting NOX2 with siRNA may provide insight as to whether the increase in NOX2 contributes to the accumulation of ROS induced by the DIM plus DOC combination.
Recent efforts in drug discovery on vascular inflammation and consequent atherosclerosis
Published in Expert Opinion on Drug Discovery, 2021
Alma Martelli, Valentina Citi, Vincenzo Calderone
Dihydromyricetin also known as ampelopsin, is a flavonoid extracted from the plant Ampelopsis grossedentata (Hand.-Mazz.). It has been reported to mediate several pharmacological activities, including hepatoprotective, antioxidant, anti-inflammatory, and lipid regulatory effects. Dihydromyricetin protected endothelial cells against palmitic acid damage, preventing caspase-1-dependent pyroptotic cell death, a highly inflammatory form of programmed cell death. In particular, dihydromyricetin treatment significantly abolished caspase-1 cleavage and consequently reduced IL-1β release, improving cell membrane integrity. Furthermore, it limited intracellular ROS formation by activating Nrf-2 antioxidant machinery. This mechanism of action has been confirmed, since the silencing of Nrf2 with specific siRNA completely abolished the protective effect of dihydromyricetin, leading to a marked increase of ROS production and pyroptotic cell death [145]. The anti-atherosclerosis effect of dihydromyricetin has been confirmed in high-fat-diet-induced atherosclerosis using LDL receptor-deficient mice. Indeed, dihydromyricetin-mediated beneficial effects improving endothelial functionality, since it normalized physiological serum lipid levels and limited vascular inflammation due to the inhibition of ox-LDL, IL-6, and TNF-α production. This reduced monocyte adhesion and oxidative stress damage, slowed down atherosclerotic lesion formation and increased plaque stability, by inhibiting macrophage foam cell formation and enhancing cholesterol efflux. At the hepatic level, dihydromyricetin limited lipid accumulation and promoted protein expressions of PPARα, LXRα, and ABCA1, normalizing ROS levels [146].
Effects of CLIC4 on Fucoxanthinol-Induced Apoptosis in Human Colorectal Cancer Cells
Published in Nutrition and Cancer, 2021
Reo Yokoyama, Hiroyuki Kojima, Rie Takai, Tohru Ohta, Hayato Maeda, Kazuo Miyashita, Michihiro Mutoh, Masaru Terasaki
Recently, we demonstrated the anticancer mechanisms of Fx and FxOH in CRC. One group demonstrated that CLIC4 could be regulated by a food component In Vivo. Cotreatment with ampelopsin, a dietary plant polyphenol having anticancer properties, with irinotecan, downregulated CLIC4, Cyclin D1, and TGF-β in cancer tissue in an azoxymethane/dextrane sodium sulfate (AOM/DSS)-treated mouse colon carcinogenic model (26). Thus, CLIC4 could be a key molecule for cancer chemoprevention/chemotherapy strategy. In this study, we examined the effects of FxOH on CLIC4 in human CRC cells.