Protective Effects Of Ginsenoside Rb1 Research Articles

Protective effect of ginsenoside Rb1 on β-amyloid protein(1-42)-induced neurotoxicity in cortical neurons

The effects of ginsenosides were thought to prevent neurodegenerative processes associated with aging. The accumulation of β-amyloid protein (Aβ) within the brain is one of the pathological hallmarks of Alzheimer's disease (AD). There is no one effective treatment of AD. To investigate the effects of ginsenoside Rb1 (GRb1) on neuronal damage induced by Aβ and potential mechanisms of the effects of GRb1 in vitro, morphological observation and biochemical analysis combining primary cultured neurons were adopted. A positive control was pre-treated with Trolox. Neurons that were treated with Aβ 1-42 (2 μM) were shrunken perikaryon with loss of neurite processes; the survival rate of neurons decreased almost to 50% (p<0.01). Lactate dehydrogenase (LDH) release, malondialdehyde (MDA) product and superoxide dismutase (SOD) activity level all increased obviously (p<0.01 or p<0.05). However, neurons pre-treated with GRb1 (0.1, 1 and 10 μM) or Trolox (10 μM) had a survival rate increase compared with neurons treated with Aβ alone; LDH release and MDA product decreased distinctly, and the increase in SOD activity in Aβ-treated neurons was attenuated evidently (p<0.01 or p<0.05). Thus, we conclude that GRb1 exerted neuroprotection obviously. GRb1 protected neurons against the toxicity of Aβ, most likely through an antioxidant pathway. GRb1 could be useful neuroprotective agents of AD.

Protective effects of ginsenoside Rb1, ginsenoside Rg1, and notoginsenoside R1 on lipopolysaccharide-induced microcirculatory disturbance in rat mesentery

Ginsenoside Rb1 (Rb1), ginsenoside Rg1 (Rg1), and notoginsenoside R1 (R1) are major active components of Panax notoginseng, a Chinese herb that is widely used in traditional Chinese medicine to enhance blood circulation and dissipate blood stasis. To evaluate the effect of these saponins on microcirculatory disturbance induced by lipopolysaccharide (LPS), vascular hemodynamics in rat mesentery was observed continuously during their administration using an inverted microscope and a high speed video camera system. LPS administration decreased red blood cell velocity but Rb1, Rg1, and R1 attenuated this effect. LPS administration caused leukocyte adhesion to the venular wall, mast cell degranulation, and the release of cytokines. Rb1, Rg1, and R1 reduced the number of adherent leukocytes, and inhibited mast cell degranulation and cytokine elevation. In vitro experiments using flow cytometry further demonstrated that a) the LPS-enhanced expression of CD11b/CD18 by neutrophils was significantly depressed by Rb1 and R1, and b) hydrogen peroxide (H 2O 2) release from neutrophils in response to LPS stimulation was inhibited by treatment with Rg1 and R1. These results suggest that the protective effect of Rb1 and R1 against leukocyte adhesion elicited by LPS may be associated with their suppressive action on the expression of CD11b/CD18 by neutrophils. The protective effect against mast cell degranulation by Rb1 and R1, and the blunting of H 2O 2 release from neutrophils by Rg1 and R1 suggest mechanistic diversity in the effects of Panax notoginseng saponins in the attenuation of microcirculatory disturbance induced by LPS.

Ginsenoside Rb1 protects against damage to the spiral ganglion cells after cochlear ischemia

The effects of transient cochlear ischemia on spiral ganglion cells (SGCs) were studied in Mongolian gerbils. Ischemic insult was induced by occluding the bilateral vertebral arteries of gerbils for 15 min. Seven days after ischemia, the percentage of SGCs decreased to 67.5% from the preischemic baseline in the basal turn. Evaluation with immunohistochemical staining showed TUNEL-positive reactions in the SGCs with fragmented nuclei. In addition, we investigated the protective effects of ginsenoside Rb1 (gRb1) against ischemic injury to SGCs. Seven days after ischemia, the auditory brainstem response threshold shift was significantly reduced and the percentage of SGCs decreased to 90.2% from the preischemic baseline in the basal turn in the gRb1-treated group. These findings suggest that gRb1 prevented hearing loss caused by ischemic injury to SGCs in Mongolian gerbils.

Effects of Homocysteine and Ginsenoside Rb1 on Endothelial Proliferation and Superoxide Anion Production

Homocysteine (Hcy) is an independent risk factor for cardiovascular disease by its multiple effects on vascular cells and throbmosis factors, which may be involved in oxidative stress mechansims. Ginsenoside Rb1, a constituent of ginseng, bears various beneficial effects on the cardiovascular system. In the present study, we investigated the effect of Hcy on endothelial proliferation and a protective effect of ginsenoside Rb1 on the action of Hcy. We initially incubated a mouse lymph node endothelial cell line (SVEC4-10) with increasing concentrations of Hcy or for different time periods and then assessed cell proliferation by using [(3)H]-thymidine incorporation. We then incubated SVEC4-10 cells with Hcy (50 microM) for 24 h with or without Rb1 (10 microM) to examine its inhibitory effect on the proliferation. These experiments were repeated in human umbilical vein endothelial cells (HUVECs). To explore the underlying molecular mechanisms, we measured superoxide anion, a reactive oxygen species (ROS), by using dihydroethidium (DHE) staining. SVEC4-10 cells treated with Hcy (50, 100, and 200 microM) for 24 h significantly reduced cell proliferation by 43%, 42%, and 40%, respectively, as compared with control cells (P < 0.01). SVEC4-10 cells treated with Hcy (50 microM) for 12 and 24 h showed a significant reduction of cell proliferation (P < 0.05). In HUVECs, Hcy (50 microM) significantly reduced cell proliferation by 55% as compared with control cells (P < 0.05). In the presence of Rb1, Hcy-induced inhibition of cell proliferation was effectively blocked in both SVEC4-10 and HUVECs. Furthermore, Hcy (50 microM) significantly increased superoxide anion production by 23% in SVEC4-10 as compared with control cells (P < 0.05). However, in the presence of Rb1, Hcy increased superoxide anion production by only 8%, showing that RB1 almost completely blocked the effect of Hcy. Hcy significantly inhibits endothelial proliferation with increased production of superoxide anion, which is effectively blocked by ginsenoside Rb1. This study provides some new aspects of Hcy-induced endothelial dysfunction, and suggests a potential role of Rb1 to block Hcy action, which may have clinical applications.