Ginsenoside Rg1 protects neurons from hypoxic–ischemic injury possibly by inhibiting Ca2+ influx through NMDA receptors and L-type voltage-dependent Ca2+ channels

Zhang, Yunfeng; Fan, Xingjuan; Li, Xia; Peng, Liang-Liang; Wang, Guohua; Ke, Kaifu; Jiang, Zheng‐Lin

doi:10.1016/j.ejphar.2007.12.037

Cited by 66 publications

(48 citation statements)

References 42 publications

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“…3). Mounting evidence indicates that ginsenoside Rg1 exerts antioxidative effects in different conditions in vitro [4,13,18,20]. Interestingly, we observed significantly higher (P \ 0.01) levels of 8-oxo-dG in cells treated with 8-MOP/UVA than that with UVA alone (Online Resource 1).…”

Section: Resultsmentioning

confidence: 42%

Ginsenoside Rg1 protects human fibroblasts against psoralen- and UVA-induced premature senescence through a telomeric mechanism

Zhou

et al. 2012

Arch Dermatol Res

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This study was aimed to investigate the protective effects of ginsenoside Rg1 on 8-methoxypsoralen(8-MOP)/Ultraviolet A (UVA)-induced premature senescence in human fibroblasts, and the underlying mechanism. We established a stress-induced premature senescence model by 8-MOP/UVA irradiation. The aging condition was determined by histochemical staining of senescence-associated β-galactosidase (SA-β-gal). Relative telomere length was calculated by the ratio of the amount of telomere DNA versus single copy DNA by real-time polymerase chain reaction, and protein levels of p-P53, p21(WAF-1) and p16(INK-4a) were estimated by Western blotting. Compared with the 8-MOP/UVA treatment group, we found that the irradiated fibroblasts pretreated with ginsenoside Rg1 demonstrated a decrease in the expression of SA-β-gal, a downregulation in the level of senescence-associated proteins, and a deceleration in telomere shortening. Taken together, these results suggest that ginsenoside Rg1 significantly antagonizes premature senescence induced by 8-MOP/UVA in fibroblasts.

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Section: Resultsmentioning

confidence: 42%

Ginsenoside Rg1 protects human fibroblasts against psoralen- and UVA-induced premature senescence through a telomeric mechanism

Zhou

et al. 2012

Arch Dermatol Res

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“…In mammals, they play the regulatory roles in development, metabolism, neurobiology and apoptosis [158]. Due to the characteristic and similarity of structure of saponin aglycones and steroids, therefore, several pharmacological properties of saponins including anti-inflammatory, immunosuppressive and neuroprotective effects [159] as well as stimulation of adipogenesis [160] or apoptosis, are associated to interact with receptors of glucocorticoid hormones [150]. …”

Section: Molecular Effect Of Saponins On Membranesmentioning

confidence: 99%

Acetylated Triterpene Glycosides and Their Biological Activity from Holothuroidea Reported in the Past Six Decades

Bahrami

Franco

2016

Marine Drugs

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Sea cucumbers have been valued for many centuries as a tonic and functional food, dietary delicacies and important ingredients of traditional medicine in many Asian countries. An assortment of bioactive compounds has been described in sea cucumbers. The most important and abundant secondary metabolites from sea cucumbers are triterpene glycosides (saponins). Due to the wide range of their potential biological activities, these natural compounds have gained attention and this has led to their emergence as high value compounds with extended application in nutraceutical, cosmeceutical, medicinal and pharmaceutical products. They are characterized by bearing a wide spectrum of structures, such as sulfated, non-sulfated and acetylated glycosides. Over 700 triterpene glycosides have been reported from the Holothuroidea in which more than 145 are decorated with an acetoxy group having 38 different aglycones. The majority of sea cucumber triterpene glycosides are of the holostane type containing a C18 (20) lactone group and either Δ7(8) or Δ9(11) double bond in their genins. The acetoxy group is mainly connected to the C-16, C-22, C-23 and/or C-25 of their aglycone. Apparently, the presence of an acetoxy group, particularly at C-16 of the aglycone, plays a significant role in the bioactivity; including induction of caspase, apoptosis, cytotoxicity, anticancer, antifungal and antibacterial activities of these compounds. This manuscript highlights the structure of acetylated saponins, their biological activity, and their structure-activity relationships.

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“…9) In addition, Rg1 also shows a neuroprotective effect on brain ischemia by inhibition of Ca 2+ influx into primary cultured hippocampal neurons. 10) However, the anti-apoptotic effect of Rg1 on the astrocytes remains to be elucidated. In the current report, we examined the impact of Rg1 treatment in vitro using murine culture astrocytes.…”

mentioning

confidence: 99%

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

Sun¹,

Lai²,

Huang³

et al. 2014

Biological & Pharmaceutical Bulletin

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Ginsenoside Rg1 (Rg1), one of the active ingredients in Panax ginseng, has been known to regulate many cellular processes. The purpose of this study was to investigate the protective effects of Rg1 on apoptosis in mouse cultured astrocytes in vitro and a mouse model of cerebral ischemia and reperfusion in vivo. The cell apoptosis was measured by fluorescence microplate reader and xCELLigence system and the Ca 2 overload was recorded by confocal microscopy. The mitochondrial membrane potential and reactive oxygen species (ROS) were determined by flow cytometry. BALB/c mice were subjected to transient middle cerebral artery occlusion (MCAO) and randomly divided into four groups: Sham (sham-operated 0.9% saline), MCAO (MCAO 0.9% saline), Rg1-L (MCAO Rg1 20 mg/kg) and Rg1-H (MCAO Rg1 40 mg/kg). Neurological deficit scores, brain water content and infarct volume were evaluated at 24 h after reperfusion. The results showed that Rg1 significantly attenuated H 2 O 2 -induced apoptosis in astrocytes. Rg1 efficiently inhibited intracellular Ca 2 overload, loss of mitochondrial membrane potential, and ROS production in astrocytes. In vivo study, it was also observed that Rg1 markedly reduced the neurological deficit scores, brain edema, and infarct volume in the model mice. These results suggest that Rg1 possesses significant neuroprotective effects, which might be related to the prevention of astrocytes from apoptosis.

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Ginsenoside Rg1 protects neurons from hypoxic–ischemic injury possibly by inhibiting Ca2+ influx through NMDA receptors and L-type voltage-dependent Ca2+ channels

Cited by 66 publications

References 42 publications

Ginsenoside Rg1 protects human fibroblasts against psoralen- and UVA-induced premature senescence through a telomeric mechanism

Ginsenoside Rg1 protects human fibroblasts against psoralen- and UVA-induced premature senescence through a telomeric mechanism

Acetylated Triterpene Glycosides and Their Biological Activity from Holothuroidea Reported in the Past Six Decades

Protective Effects of Ginsenoside Rg1 on Astrocytes and Cerebral Ischemic-Reperfusion Mice

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