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- 저자 : Weizu Li (검색결과 3 건)
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Yuli Han,Xuewang Li,Liu Yang,Duoduo Zhang,Lan Li,Xianan Dong,Yan Li,Sen Qun,Weizu Li 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4
Background: The incidence of ischemic cerebrovascular disease is increasing in recent years and has beenone of the leading causes of neurological dysfunction and death. Ginsenoside Rg1 has been found toprotect against neuronal damage in many neurodegenerative diseases. However, the effect and mechanismby which Rg1 protects against cerebral ischemia-reperfusion injury (CIRI) are not fully understood. Here, we report the neuroprotective effects of Rg1 treatment on CIRI and its possible mechanisms inmice. Methods: A bilateral common carotid artery ligation was used to establish a chronic CIRI model in mice. HT22 cells were treated with Rg1 after OGD/R to study its effect on [Ca2þ]i. The open-field test and poleclimbingexperiment were used to detect behavioral injury. The laser speckle blood flowmeter was usedto measure brain blood flow. The Nissl and H&E staining were used to examine the neuronal damage. TheWestern blotting was used to examine MAP2, PSD95, Tau, p-Tau, NOX2, PLC, p-PLC, CN, NFAT1, and NLRP1expression. Calcium imaging was used to test the level of [Ca2þ]i. Results: Rg1 treatment significantly improved cerebral blood flow, locomotion, and limb coordination,reduced ROS production, increased MAP2 and PSD95 expression, and decreased p-Tau, NOX2, p-PLC, CN,NFAT1, and NLRP1 expression. Calcium imaging results showed that Rg1 could inhibit calcium overloadand resist the imbalance of calcium homeostasis after OGD/R in HT22 cells. Conclusion: Rg1 plays a neuroprotective role in attenuating CIRI by inhibiting oxidative stress, calciumoverload, and neuroinflammation.
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Ginsenoside Rg1 alleviates A deposition by inhibiting NADPH oxidase 2 activation in APP/PS1 mice
Han Zhang,Yong Su,Zhenghao Sun,Ming Chen,Yuli Han,Yan Li,Xianan Dong,Shixin Ding,Zhirui Fang,Weiping Li,Weizu Li 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6
Background: Ginsenoside Rg1 (Rg1), an active ingredient in ginseng, may be a potential agent for thetreatment of Alzheimer’s disease (AD). However, the protective effect of Rg1 on neurodegeneration in ADand its mechanism of action are still incompletely understood. Methods: Wild type (WT) and APP/PS1 AD mice, from 6 to 9 months old, were used in the experiment. The open field test (OFT) and Morris water maze (MWM) were used to detect behavioral changes. Neuronal damage was assessed by hematoxylin and eosin (H&E) and Nissl staining. Immunofluorescence,western blotting, and quantitative real-time polymerase chain reaction (q-PCR) were used toexamine postsynaptic density 95 (PSD95) expression, amyloid beta (Ab) deposition, Tau and phosphorylatedTau (p-Tau) expression, reactive oxygen species (ROS) production, and NAPDH oxidase 2(NOX2) expression. Results: Rg1 treatment for 12 weeks significantly ameliorated cognitive impairments and neuronaldamage and decreased the p-Tau level, amyloid precursor protein (APP) expression, and Ab generation inAPP/PS1 mice. Meanwhile, Rg1 treatment significantly decreased the ROS level and NOX2 expression inthe hippocampus and cortex of APP/PS1 mice. Conclusions: Rg1 alleviates cognitive impairments, neuronal damage, and reduce Ab deposition byinhibiting NOX2 activation in APP/PS1 mice.
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Xianan Dong,Liangliang Kong,Lei Huang,Yong Su,Xuewang Li,Liu Yang,Pengmin Ji,Weiping Li,Weizu Li The Korean Society of Ginseng 2023 Journal of Ginseng Research Vol.47 No.3
Background: As a complication of Type II Diabetes Mellitus (T2DM), the etiology, pathogenesis, and treatment of cognitive dysfunction are still undefined. Recent studies demonstrated that Ginsenoside Rg1 (Rg1) has promising neuroprotective properties, but the effect and mechanism in diabetes-associated cognitive dysfunction (DACD) deserve further investigation. Methods: After establishing the T2DM model with a high-fat diet and STZ intraperitoneal injection, Rg1 was given for 8 weeks. The behavior alterations and neuronal lesions were judged using the open field test (OFT) and Morris water maze (MWM), as well as HE and Nissl staining. The protein or mRNA changes of NOX2, p-PLC, TRPC6, CN, NFAT1, APP, BACE1, NCSTN, and Ab1-42 were investigated by immunoblot, immunofluorescence or qPCR. Commercial kits were used to evaluate the levels of IP3, DAG, and calcium ion (Ca<sup>2+</sup>) in brain tissues. Results: Rg1 therapy improved memory impairment and neuronal injury, decreased ROS, IP3, and DAG levels to revert Ca<sup>2+</sup> overload, downregulated the expressions of p-PLC, TRPC6, CN, and NFAT1 nuclear translocation, and alleviated Aβ deposition in T2DM mice. In addition, Rg1 therapy elevated the expression of PSD95 and SYN in T2DM mice, which in turn improved synaptic dysfunction. Conclusions: Rg1 therapy may improve neuronal injury and DACD via mediating PLC-CN-NFAT1 signal pathway to reduce Aβ generation in T2DM mice.
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