Abstract:As the aging phenomenon continues to increase, the incidence of neurodegenerative diseases continues to increase annually. As one of the significant contributive factors of neurodegenerative diseases, oxidative stress damage has received extensive attention in recent years. Oxidative stress plays an important role in neuronal damage through various apoptotic mechanisms related to neurodegenerative diseases. The use of natural antioxidants to combat oxidative stress may be a useful approach in delaying disease … Show more
“…Hence, Aβ42-stimulated PC12 cells presented the enhancement of Caspase-3, Caspase-9 and Bax mRNA contents and suppressed mRNA expression of Bcl-2, which indicated that hyperoside may treat AD via regulating apoptosis. This is similar to a previous report which illustrate that hyperoside could effectively reverse inhibit H 2 O 2 -stimulated damage in PC12 cells regulating apoptosisrelated genes [11]. In addition, Jia et al reported that dihydromyricetin, a natural avonoid from Ampelopsis grossedentata, attenuated Aβ40-induced neurotoxicity and apoptosis in PC12 cells [40].…”
Section: Discussionsupporting
confidence: 89%
“…Hyperoside is a avonoid existing in a variety of medicinal plants including Acanthopanax senticosus and Hypericum [9]. Recently, many studies have indicated that hyperoside possessed different biological activities such as inhibiting apoptosis, anti-oxidation, and anti-in ammatory etc [10,11]. In addition, hyperoside suppressed neuroin ammation by inhibiting TNF-α/NF-κB/caspase-3 pathways in type 2 diabetes rats [12].…”
Traditional Chinese medicines such as hyperoside-rich Acanthopanax senticosus and Crataegus pinnatifida have been confirmed to exhibit anti-oxidative stress properties. Hyperoside, the main ingredient of numerous antioxidant herbs, may have the ability to postpone the onset of neurodegenerative diseases This study investigates the possible therapeutic mechanism of hyperoside as a natural antioxidant against Alzheimer’s disease (AD) in Caenorhabditis elegans and PC12 cells. Specifically, hyperoside reduced reactive oxygen species (ROS) level and Aβ42-induced neurotoxicity in C. elegans worms. Meanwhile, hyperoside reduced ROS production and increased mitochondrial membrane potentialin Aβ42-induced PC12 cells, which possibly due to the increase of antioxidant enzymes activity and the diminution of malondialdehyde levels. Hoechst 33342 staining and real-time PCR results suggested that hyperoside reverses cell apoptosis. Network pharmacology predicts potentially relevant hypericin targets and pathways in AD therapy. As anticipated, hyperoside reversed Aβ42-stimulated downregulation of the PI3K/Akt/Nrf2/HO-1. The PI3K inhibitor LY294002 partially abolished the protective capability of hyperoside. The results of molecular docking further indicated that the PI3K/Akt pathways may be involved in the protection of Aβ42-induced PC12 cells by hyperoside treatment. The study provides theoretical information for research and development of hyperoside as an antioxidant dietary supplement.
“…Hence, Aβ42-stimulated PC12 cells presented the enhancement of Caspase-3, Caspase-9 and Bax mRNA contents and suppressed mRNA expression of Bcl-2, which indicated that hyperoside may treat AD via regulating apoptosis. This is similar to a previous report which illustrate that hyperoside could effectively reverse inhibit H 2 O 2 -stimulated damage in PC12 cells regulating apoptosisrelated genes [11]. In addition, Jia et al reported that dihydromyricetin, a natural avonoid from Ampelopsis grossedentata, attenuated Aβ40-induced neurotoxicity and apoptosis in PC12 cells [40].…”
Section: Discussionsupporting
confidence: 89%
“…Hyperoside is a avonoid existing in a variety of medicinal plants including Acanthopanax senticosus and Hypericum [9]. Recently, many studies have indicated that hyperoside possessed different biological activities such as inhibiting apoptosis, anti-oxidation, and anti-in ammatory etc [10,11]. In addition, hyperoside suppressed neuroin ammation by inhibiting TNF-α/NF-κB/caspase-3 pathways in type 2 diabetes rats [12].…”
Traditional Chinese medicines such as hyperoside-rich Acanthopanax senticosus and Crataegus pinnatifida have been confirmed to exhibit anti-oxidative stress properties. Hyperoside, the main ingredient of numerous antioxidant herbs, may have the ability to postpone the onset of neurodegenerative diseases This study investigates the possible therapeutic mechanism of hyperoside as a natural antioxidant against Alzheimer’s disease (AD) in Caenorhabditis elegans and PC12 cells. Specifically, hyperoside reduced reactive oxygen species (ROS) level and Aβ42-induced neurotoxicity in C. elegans worms. Meanwhile, hyperoside reduced ROS production and increased mitochondrial membrane potentialin Aβ42-induced PC12 cells, which possibly due to the increase of antioxidant enzymes activity and the diminution of malondialdehyde levels. Hoechst 33342 staining and real-time PCR results suggested that hyperoside reverses cell apoptosis. Network pharmacology predicts potentially relevant hypericin targets and pathways in AD therapy. As anticipated, hyperoside reversed Aβ42-stimulated downregulation of the PI3K/Akt/Nrf2/HO-1. The PI3K inhibitor LY294002 partially abolished the protective capability of hyperoside. The results of molecular docking further indicated that the PI3K/Akt pathways may be involved in the protection of Aβ42-induced PC12 cells by hyperoside treatment. The study provides theoretical information for research and development of hyperoside as an antioxidant dietary supplement.
“…This CAA through diverse pathways, including lowering intracellular ROS generation ( Gao et al, 2019 ), enhancing antioxidant defences via the mitogen-activated protein kinase (MAPK)-dependent Kelch-like ECH Homology (ECH)-associated protein 1 (Keap 1)-nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) signaling pathway ( Xing et al, 2011 ), and activating enzymes, such as heme oxygenase-1 (HO-1) through the activation of the Nrf2-extracellular signal-regulated kinase (ERK) signaling pathway ( Park et al, 2016 ). These mechanisms protect cells from oxidative stress by regulating inflammation, autophagy, and apoptosis-related pathways in response to hydrogen peroxide-induced oxidative stress ( Feng et al, 2021 ). Fig.…”
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