Ginsenoside Rg1 attenuates motor impairment and neuroinflammation in the MPTP-probenecid-induced parkinsonism mouse model by targeting α-synuclein abnormalities in the substantia nigra

Heng, Yang; Zhang, Qiu-Shuang; Zheng, Ming; Hu, Jin‐Feng; Yuan, Yu‐He; Chen, Nai‐Hong

doi:10.1016/j.toxlet.2015.12.005

Cited by 75 publications

(69 citation statements)

References 70 publications

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“…After full-text evaluation on the remaining 67 articles, 11 articles were removed because of combination with other treatment drugs in the experimental group; 23 articles were excluded because they did not test the efficacy of G-Rg1 on PD animals; 8 articles were excluded because of duplicate publication. Eventually, 25 eligible studies [16–40] were identified (Figure 1). …”

Section: Resultsmentioning

confidence: 99%

“…The weight of C57BL/6 mice varied from 16 g to 30 g, and the weight of ovariectomized Wistar rats varied from 200 g to 250 g. Eight articles [16–20, 35, 39, 40] were published in English academic journals and 17 articles [21–34, 36–38] were published in Chinese academic journals from 2001 to 2016. As for experimental animal model, twenty studies used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced PD model [16–34, 39], 4 studies [35–38] used 6-hydroxydopamine (6-OHDA) induced PD model, and 1 study used lipopolysaccharide- (LPS-) induced PD model [40]. In terms of gender, five studies [25, 35, 37, 38, 40] used merely female animals and eighteen studies [16, 18–20, 22–24, 26–34, 36, 39] used merely male animals, while the remaining 2 studies [17, 21] did not report gender.…”

Section: Resultsmentioning

confidence: 99%

“…As for experimental animal model, twenty studies used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced PD model [16–34, 39], 4 studies [35–38] used 6-hydroxydopamine (6-OHDA) induced PD model, and 1 study used lipopolysaccharide- (LPS-) induced PD model [40]. In terms of gender, five studies [25, 35, 37, 38, 40] used merely female animals and eighteen studies [16, 18–20, 22–24, 26–34, 36, 39] used merely male animals, while the remaining 2 studies [17, 21] did not report gender. Among 25 included studies, one study used ether cotton balls to induce anesthesia [33], two studies used urethane [17, 26], eleven studies used chloral hydrate [16, 23, 27, 28, 30, 32, 35–38, 40], four studies used pentobarbital sodium [18, 20, 31, 39], three studies did not report anesthesia [24, 29, 34], and the remaining four studies did not report the method of executing the animals [19, 21, 22, 25].…”

Section: Resultsmentioning

confidence: 99%

“…For all included studies, the intervention measures for experimental groups were injection with G-Rg1 before injection of MPTP, 6-OHDA, or LPS. Fifteen studies used behavioral assessments as primary outcomes [16, 17, 22–24, 26, 28, 29, 32–37, 39]. TH-positive dopamine neurons in the SNpc were observed in 16 studies [16–20, 24, 26, 28–32, 34, 35, 38, 39].…”

Section: Resultsmentioning

confidence: 99%

“…Fifteen studies used behavioral assessments as primary outcomes [16, 17, 22–24, 26, 28, 29, 32–37, 39]. TH-positive dopamine neurons in the SNpc were observed in 16 studies [16–20, 24, 26, 28–32, 34, 35, 38, 39]. Nine studies reported the levels of TH protein expression [16, 18, 22–24, 29, 30, 32, 34].…”

Section: Resultsmentioning

confidence: 99%

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A Preclinical Systematic Review of Ginsenoside-Rg1 in Experimental Parkinson’s Disease

Song

Zhou

et al. 2017

Oxidative Medicine and Cellular Longevity

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To date, no drug has been proven to be neuroprotective or disease-modifying for Parkinson's disease (PD) in clinical trials. Here, we aimed to assess preclinical evidence of Ginsenosides-Rg1 (G-Rg1), a potential neuroprotectant, for experimental PD and its possible mechanisms. Eligible studies were identified by searching six electronic databases from their inception to August 2016. Twenty-five eligible studies involving 516 animals were identified. The quality score of these studies ranged from 3 to 7. Compared with the control group, two out of the 12 studies of MPTP-induced PD showed significant effects of G-Rg1 for improving the rotarod test (P < 0.01), two studies for improving the swim-score values (P < 0.01), six studies for improving the level of TH protein expression (P < 0.01), and two studies for increasing the expression of TH mRNA in the substantia nigra of mice (P < 0.01). The studies reported that G-Rg1 exerted potential neuroprotective effects on PD model through different mechanisms as antineuroinflammatory activities (n = 10), antioxidant stress (n = 3), and antiapoptosis (n = 11). In conclusion, G-Rg1 exerted potential neuroprotective functions against PD largely by antineuroinflammatory, antioxidative, and antiapoptotic effects. G-Rg1 as a promising neuroprotectant for PD needs further confirmation by clinical trials.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 3 more Smart Citations

A Preclinical Systematic Review of Ginsenoside-Rg1 in Experimental Parkinson’s Disease

Song

Zhou

et al. 2017

Oxidative Medicine and Cellular Longevity

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Effects of Ginsenoside Rg1 on Learning and Memory in a Reward‐directed Instrumental Conditioning Task in Chronic Restraint Stressed Rats

Wang

Lü

et al. 2016

Phytotherapy Research

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Ginsenoside Rg1 is one of the major active ingredients of Panax ginseng and has showed notable improving learning and memory effects in several behavioral tasks, such as water maze, shuttle-box, and step-through, based on avoidance. However, there was no report about the role of Rg1 on the performance of reward-directed instrumental conditioning, which could reflect the adaptive capacity to ever-changing environments. Thus, in this study, the reward devaluation test and conditional visual discrimination task were conducted to study the ameliorating effects of Rg1 on cognitive deficits, especially the loss of adaptation capacity in chronic restraint stress (CRS) rat model. Our results showed that rat subjected to CRS became insensitive to the changes in outcome value, and it significantly harmed the rat's performance in conditional visual discrimination task. Moreover, the levels of BDNF, TrkB, and Erk phosphorylation were decreased in the prefrontal cortex of CRS rats. However, these changes were effectively reversed by Rg1 (5 and 10 mg/kg, i.p.). Therefore, it demonstrated that Rg1 has a good ability to improve learning and memory and also ameliorate impaired adaptive capacity induced by CRS. This amelioration effect of Rg1 might be mediated partially by BDNF/TrkB/Erk pathway in prefrontal cortex. Copyright © 2016 John Wiley & Sons, Ltd.

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Ginsenoside Rg3 and Rh2 protect trimethyltin‐induced neurotoxicity via prevention on neuronal apoptosis and neuroinflammation

Hou

Xue

Wang

et al. 2018

Phytotherapy Research

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The acute exposure of trimethyltin (TMT) develops clinical syndrome characterized by amnesia, aggressive behavior, and complex seizures. This neurotoxicant selectively induces hippocampal neuronal injury and glial activation accompanied with resultant neuroinflammation. Here we report two candidates ginsenosides Rg3 and Rh2 as neuroprotection agents using a mouse model of TMT intoxication via a single injection (2 mg/kg) and primary neuronal culture systems. Four-week administration of Rg3 or Rh2 significantly reduced TMT-induced seizures and behavioral changes. Rg3 and Rh2 significantly attenuated the oxidative stress evidenced by improvement on antioxidant enzymes and neuronal loss and astrocytic activation in mouse brain. In primary cultures, TMT induced significant neuronal death after 24-h intoxication and vigorous secretion of inflammatory cytokines (IL-1α/β, IL-6, TNF-α, and MCP-1) in astrocytes. Pretreatment with Rg3 or Rh2 not only reduced cell death but efficiently suppressed above mentioned inflammatory cytokines confirmed by antibody array test. The underlying protective mechanism by Rg3 and Rh2 was delineated through selective upregulation of PI3K/Akt and suppression of ERK activation. Intriguingly, Rg3 and Rh2 protected oligodendrocyte progenitor cells (O-2A) from TMT intoxication via promoting type 2 astrocytic differentiation without further inflammatory activation. Collectively, Rg3 and Rh2 interventions aimed at reducing oxidative stress and neuroinflammation neurotoxicity therefore are of therapeutic benefit in TMT-induced neurodegeneration. KEYWORDS neuroinflammation, oligodendrocyte progenitor cells (O-2A), oxidative stress, Rg3 and Rh2, TMT

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Ginsenoside Rg1 attenuates motor impairment and neuroinflammation in the MPTP-probenecid-induced parkinsonism mouse model by targeting α-synuclein abnormalities in the substantia nigra

Cited by 75 publications

References 70 publications

A Preclinical Systematic Review of Ginsenoside-Rg1 in Experimental Parkinson’s Disease

A Preclinical Systematic Review of Ginsenoside-Rg1 in Experimental Parkinson’s Disease

Effects of Ginsenoside Rg1 on Learning and Memory in a Reward‐directed Instrumental Conditioning Task in Chronic Restraint Stressed Rats

Ginsenoside Rg3 and Rh2 protect trimethyltin‐induced neurotoxicity via prevention on neuronal apoptosis and neuroinflammation

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