Ginsenoside Rb1 as a neuroprotective agent: A review

Ahmed, Touqeer; Raza, Syed Hammad; Maryam, Afifa; Setzer, William N.; Braidy, Nady; Nabavi, Seyed Fazel; Oliveira, Marcos Roberto de

doi:10.1016/j.brainresbull.2016.04.002

Cited by 126 publications

(71 citation statements)

References 119 publications

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“…Moreover, the antioxidant and anti-inflammatory effects have also been shown to be implicated in the neuroprotective effects of both Rb1 and Rd 15, 33, 34 . For instance, in addition to maintaining the balance of pro- and antioxidant mechanisms, Rd significantly attenuates the inflammatory responses in carrageenan-induced rat paw edema in part through suppressing proinflammatory ERK/JNK/NF-κB signaling 32 .…”

Section: Discussionmentioning

confidence: 99%

Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration

Bian

Wang

et al. 2017

Sci Rep

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Photoreceptor degeneration is a central pathology of various retinal degenerative diseases which currently lack effective therapies. Antioxidant and anti-inflammatory activities are noted for Panax notoginsenoside saponins (PNS) and related saponin compound(s). However, the photoreceptor protective potentials of PNS or related saponin compound(s) remain unknown. The current study revealed that PNS protected against photoreceptor loss in bright light-exposed BALB/c mice. Combination of ginsenoside Rb1 and Rd, two major saponin compounds of PNS, recapitulated the retinal protection of PNS and attenuated retinal oxidative stress and inflammatory changes. Rb1 or Rd partially alleviated all-trans-Retinal-induced oxidative stress in ARPE19 cells. Rb1 or Rd suppressed lipopolysaccharides (LPS)-induced proinflammatory gene expression in ARPE19 and RAW264.7 cells. Rb1 or Rd also modulated the expression of proinflammatory microRNA, miR-155 and its direct target, anti-inflammatory SHIP1, in LPS-stimulated RAW264.7 cells. The retinal expression of miR-155 and SHIP1 was altered preceding extensive retinal damage, which was maintained at normal level by Rb1 and Rd combination. This work shows for the first time that altered expression of miR-155 and SHIP1 are involved in photoreceptor degeneration. Most importantly, novel retinal protective activities of combination of Rb1 and Rd justify further evaluation for the treatment of related retinal degenerative disorders.

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Section: Discussionmentioning

confidence: 99%

Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration

Bian

Wang

et al. 2017

Sci Rep

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“…Mey, have been reported to elicit pharmacological effects, such as immunoregulation, neuroprotection, and hepatoprotection [6,7]. Many studies have demonstrated that ginsenosides can function as hepatoprotective agents in multiple models of hepatic injury and other diseases [6,7]. However, the protective mechanism of Rg1 and Rb1 in CCl 4 -induced liver injury is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective effects of ginseng saponins in a mouse model of carbon tetrachloride-induced liver injury

Lu¹,

Tan²,

Yang³

et al. 2019

Trop. J. Pharm Res

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Purpose: To investigate the effects of ginsenosides Rg1 and Rb1 on carbon tetrachloride (CCl4)induced liver injury in mice. Methods: Thirty-two mice were randomly divided into four groups. In control group, mice were administered sodium carboxymethylcellulose (CMC-Na) by intraperitoneal injection for seven days. In CCl4 treatment group, mice were treated as control group for the first seven days and then intraperitoneally injected with CCl4 in olive oil on day 8. In Rb1-and Rg1-treatment group, the mice were intraperitoneally injected with Rb1 or Rg1 (each 30 mg/kg, dissolved in 0.5 % CMC-Na), respectively for seven days, followed by intraperitoneal injection with CCl4 in olive oil on day 8. Histological damage was examined by haematoxylin and eosin (H&E) staining. Serum levels of alanine aminotransferase (ALT) and aspartate transaminase (AST) were assessed enzymatically. Tissue IL-6 and IL-8 levels were measured by ELISA. Gene and protein levels of transforming growth factor (TGF)-β, Smad2, and Smad3 were analyzed by real-time PCR (RT-PCR) and western blotting, respectively. Results: CCl4 treatment caused histological damage in mouse liver, and increased the levels of ALT, AST (five-fold), IL-6 (three-fold), and IL-8 (five-fold), and elevated expressions of TGF-β, Smad2, and Smad3. Ginsenosides Rg1 or Rb1 pre-treatment attenuated liver injury by decreasing the serum levels of ALT (from 700 to 200 UI/L) AST (from 550 pg/mL to 250 pg/ml), IL-6 (from 1,100 to 750 pg/mL), and IL-8 (from 600 to 200 pg/mL), and inhibiting the expressions of TGF-β, Smad2, and Smad3. Conclusion: Ginsenosides (Rg1 and Rb1) attenuate CCl4-induced liver injury and inflammation by regulating TGF-β/Smad signalling pathway.

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“…Ginseng has been used for more than 2,000 years as a traditional medicine in Asian countries [1, 2]. Ginsenosides, the major active components from stems and leaves of Panax ginseng, have been reported to show various protective effects on ischemic brain injury [3-5].…”

Section: Introductionmentioning

confidence: 99%

Involvement of N-Methyl-D-Aspartic Acid Receptor and DL-α-Amino-3-Hydroxy-5- Methyl-4-Isoxazole Propionic Acid Receptor in Ginsenosides Rb1 and Rb3 against Oxygen-Glucose Deprivation-Induced Injury in Hippocampal Slices from Rat

Jiang¹,

Fang²,

Chen

2017

Pharmacology

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Objective: Ginsenosides, Rb1 and Rb3, are the major protopanaxadiol components of ginseng saponin. In the present study, the influences of ginsenosides Rb1 and Rb3 on N-methyl-D-aspartic acid (NMDA) receptor or DL-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated synaptic transmission after oxygen-glucose deprivation (OGD) were investigated. Methods: NMDA receptor population spike (NMDA-PS) or AMPA receptor-mediated population spike (AMPA-PS) was recorded in the CA1 pyramidal cell layer of rat hippocampal slices by electrophysiological techniques. Results: Under normal conditions, ginsenosides Rb3 and Rb1 depressed glutamate receptors-mediated synaptic transmission. Fourteen min of OGD resulted in a poor recovery amplitude of NMDA-PS or AMPA-PS after reoxygenation. Ginsenoside Rb3 significantly delayed the appearance of transient recovery of PS during OGD, and improved the recovery amplitudes of NMDA-PS and AMPA-PS after reoxygenation. However, the similar protective effects of ginsenoside Rb1 were observed only on NMDA-PS but not AMPA-PS. Conclusion: These results suggest that ginsenosides Rb1 and Rb3 have the different inhibitions on NMDA and AMPA receptors-mediated response, which may partially explain the different protective effects of these agents on ischemic neuronal death.

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Ginsenoside Rb1 as a neuroprotective agent: A review

Cited by 126 publications

References 119 publications

Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration

Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration

Hepatoprotective effects of ginseng saponins in a mouse model of carbon tetrachloride-induced liver injury

Involvement of N-Methyl-D-Aspartic Acid Receptor and DL-α-Amino-3-Hydroxy-5- Methyl-4-Isoxazole Propionic Acid Receptor in Ginsenosides Rb1 and Rb3 against Oxygen-Glucose Deprivation-Induced Injury in Hippocampal Slices from Rat

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