Hyperoside protects against chronic mild stress-induced learning and memory deficits

Gong, Yeli; Yang, Youhua; Chen, Xiaoqing; Huang, Dan; Yang, Rong; Zhou, Lianying; Li, Changlei; Xiong, Qiuju; Xiong, Zhe

doi:10.1016/j.biopha.2017.05.019

Cited by 38 publications

(12 citation statements)

References 42 publications

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“…Hyperoside (quercetin 3- O -galactoside), a phenolic compound present in the bark of A. tegmentosum , has displayed multiple biological protective effects against chronic diseases through its antioxidant [47], anti-inflammatory [48] and anticancer [49] activities; moreover, it effectively prevents amyloid beta-induced neurotoxicity [50], oxygen-glucose deprivation-reperfusion-induced cortical neuron injury [51] and chronic stress-exposed depressive-like behavior [52] in vivo. There is growing evidence of the effects of hyperoside on neurodegenerative diseases; however, the mechanisms underlying these effects of hyperoside in PD have not yet been addressed.…”

Section: Discussionmentioning

confidence: 99%

Suppression of 6-Hydroxydopamine-Induced Oxidative Stress by Hyperoside Via Activation of Nrf2/HO-1 Signaling in Dopaminergic Neurons

Kwon

Lee

Park

et al. 2019

IJMS

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In our ongoing research to discover natural products with neuroprotective effects, hyperoside (quercetin 3-O-galactoside) was isolated from Acer tegmentosum, which has been used in Korean traditional medicine to treat liver-related disorders. Here, we demonstrated that hyperoside protects cultured dopaminergic neurons from death via reactive oxygen species (ROS)-dependent mechanisms, although other relevant mechanisms of hyperoside activity remain largely uncharacterized. For the first time, we investigated the neuroprotective effects of hyperoside on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in neurons, and the possible underlying mechanisms. Hyperoside significantly ameliorated the loss of neuronal cell viability, lactate dehydrogenase release, excessive ROS accumulation and mitochondrial membrane potential dysfunction associated with 6-OHDA-induced neurotoxicity. Furthermore, hyperoside treatment activated the nuclear erythroid 2-related factor 2 (Nrf2), an upstream molecule of heme oxygenase-1 (HO-1). Hyperoside also induced the expression of HO-1, an antioxidant response gene. Remarkably, we found that the neuroprotective effects of hyperoside were weakened by an Nrf2 small interfering RNA, which blocked the ability of hyperoside to inhibit neuronal death, indicating the vital role of HO-1. Overall, we show that hyperoside, via the induction of Nrf2-dependent HO-1 activation, suppresses neuronal death caused by 6-OHDA-induced oxidative stress. Moreover, Nrf2-dependent HO-1 signaling activation represents a potential preventive and therapeutic target in Parkinson′s disease management.

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Section: Discussionmentioning

confidence: 99%

Suppression of 6-Hydroxydopamine-Induced Oxidative Stress by Hyperoside Via Activation of Nrf2/HO-1 Signaling in Dopaminergic Neurons

Kwon

Lee

Park

et al. 2019

IJMS

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“…Hyperoside (HYP), chemical name is quercetin 3-O-b-D-galactoside, which belongs to the flavonol glycosides [8]. Since HP possess the presence of alcoholic hydroxyl groups in the molecule, and is widely present in plants such as Campanulaceae and Rosaceae.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of hyperoside against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells

Qi¹,

Лі²,

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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Oxidative stress can induce apoptosis and decrease activities of osteoblasts. Hyperoside (HYP) is a potent antioxidant derived from Chinese herb. This study aims to evaluate the protective effects provided by HYP to osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were pre-treated with HYP for 24 h before being treated with 0.3 mM hydrogen peroxide (H 2 O 2) for 24 h. Cell viability, flow cytometric analysis and mRNA expression of alkaline phosphatase (ALP), collagen I (COL-I) and osteocalcin (OCN) in MC3T3-E1 cells were examined. We next examined apoptosis-related and mitogen-activated protein kinase (MAPK) related proteins in HYP and H 2 O 2 groups. HYP over the dose of 40 lmol/L could obviously increase the MC3T3-E1 cell viability at 24 h and 48 h (p < .05). HYP significantly (p < .05) increased mRNA expression of ALP, COL-I and OCN than H 2 O 2 group. Moreover, HYP decreased the apoptosis rate and apoptosis-related proteins that induced by H 2 O 2. In addition, HYP decreased the production of phosphorylated Jun N-terminal kinase (JNK) and p38 levels of osteoblastic MC3T3-E1 cells induced by H 2 O 2. These results demonstrated that the protective effect provided by HYP to osteoblastic MC3T3-E1 cells was mediated, at least in part, via inhibition of MAPK signalling pathway and oxidative damage of the cells.

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“…Zhang et al demonstrated that emodin inhibited excess inflammatory response by targeting miR-139-5p/5-lipoxygenase ( Zhang et al, 2021 ). Hyperoside increased the expression of BDNF in the hippocampus of CUMS rats, but it did not affect the level of plasma corticosterone (CORT), so it may be one of the potential reasons for the antidepressant effect of Hypericum perforatum ( Gong et al, 2017 ).…”

Section: Molecular Mechanism Of Action Of Sg Antidepressantsmentioning

confidence: 99%

Shugan Jieyu Capsule in Post-Stroke Depression Treatment: From Molecules to Systems

Zhang

Bai

2022

Front. Pharmacol.

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Post-stroke depression (PSD) is the most common non-cognitive neuropsychiatric complication after stroke, and about a third of patients with stroke have depression. Although a great deal of effort has been made to treat PSD, the efficacy thereof has not been satisfactory, due to the complex pathological mechanism underlying PSD. In Traditional Chinese Medicine (TCM) theory, PSD is considered to be a combination of “stroke” and “Yu Zheng.” The holistic, multi-drug, and multi-objective nature of TCM is consistent with the treatment concept of systems medicine for PSD. TCM has a very long history of being used to treat depression, and various TCM prescriptions have been clinically proven to be effective in improving depression. Among the numerous prescriptions for treating depression, Shugan Jieyu capsule (SG) is one of the classic prescriptions. Additionally, clinical studies have increasingly confirmed that using SG alone or in combination with Western medicine can significantly improve the psychiatric symptoms of PSD patients. Here, we reviewed the mechanism of antidepressant action of SG and its targets in PSD pathologic systems. This review provides further insights into the pharmacological mechanism, drug interaction, and clinical application of TCM prescriptions, as well as a basis for the development of new drugs to treat PSD.

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Hyperoside protects against chronic mild stress-induced learning and memory deficits

Cited by 38 publications

References 42 publications

Suppression of 6-Hydroxydopamine-Induced Oxidative Stress by Hyperoside Via Activation of Nrf2/HO-1 Signaling in Dopaminergic Neurons

Suppression of 6-Hydroxydopamine-Induced Oxidative Stress by Hyperoside Via Activation of Nrf2/HO-1 Signaling in Dopaminergic Neurons

Protective effect of hyperoside against hydrogen peroxide-induced dysfunction and oxidative stress in osteoblastic MC3T3-E1 cells

Shugan Jieyu Capsule in Post-Stroke Depression Treatment: From Molecules to Systems

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