• The Journal of Korean Medicine
• /
• v.20 no.1 s.37
• /
• pp.161-171
• /
• 1999

This study was performed to investigate the effect of complex formula(CKRG) consisting of Panax ginseng Radix rubra Koreana. Ganoderma, Cinnamomi Cortex, Glycyrrhizae Radix and Laminariae Thallus on brain ischemia and injury such as KCN-induced brain injury, forced brain ischemia, pulmonary thrombosis. The results were summarized as follows: 1. CKRG extracts showed a decrease of the duration of KCN-induced coma and showcd an increase in life expectancy. 2. CKRG extracts showed a decrease of neurologic grade in hind limb but did not affect neurologic grades in fore limb. Also. CKRG extracts showed a significant decrease of brain ischemic area and edema in MCA occlusion, 3. CKRG extracts showed a protective effect on pulmonary thrombosis induced by collagen and epinephrine. These data suggested that CKRG extracts could be applied to the protection of brain ischemia and injury.

• Journal of Ginseng Research
• /
• v.46 no.5
• /
• pp.621-627
• /
• 2022

Background: Panax ginseng (ginseng) is a traditional medicine that is reported to have cardioprotective effects; ginsenosides are the major bioactive compounds in the ginseng root. Methods: Magnetic molecularly imprinted polymer (MMIP) nanoparticles might be useful for both the extraction of the targeted (imprinted) molecules, and for the delivery of those molecules to cells. In this work, plant growth regulators were used to enhance the adventitious rooting of ginseng root callus; imprinted polymeric particles were synthesized for the extraction of ginsenoside Rb₁ from root extracts, and then employed for subsequent particle-mediated delivery to cardiomyocytes to mitigate hypoxia/reoxygenation injury. Results: These synthesized composite nanoparticles were first characterized by their specific surface area, adsorption capacity, and magnetization, and then used for the extraction of ginsenoside Rb₁ from a crude extract of ginseng roots. The ginsenoside-loaded MMIPs were then shown to have protective effects on mitochondrial membrane potential and cellular viability for H9c2 cells treated with CoCl₂ to mimic hypoxia injury. The protective effect of the ginsenosides was assessed by staining with JC-1 dye to monitor the mitochondrial membrane potential. Conclusion: MMIPs can play a dual role in both the extraction and cellular delivery of therapeutic ginsenosides.

• Journal of Ginseng Research
• /
• v.40 no.3
• /
• pp.278-284
• /
• 2016

Background: The ginsenoside Rb1 (Rb1) is the most abundant compound in the root of Panax ginseng. Recent studies have shown that Rb1 has a neuroprotective effect. However, the mechanisms underlying this effect are still unknown. Methods: We used stable isotope labeling with amino acids in cell culture, combined with quantitative mass spectrometry, to explore a potential protective mechanism of Rb1 in ${\beta}$-amyloid-treated neuronal cells. Results: A total of 1,231 proteins were commonly identified from three replicate experiments. Among these, 40 proteins were significantly changed in response to Rb1 pretreatment in ${\beta}$-amyloid-treated neuronal cells. Analysis of the functional enrichments and protein interactions of altered proteins revealed that actin cytoskeleton proteins might be linked to the regulatory mechanisms of Rb1. The CAP1, CAPZB, TOMM40, and DSTN proteins showed potential as molecular target proteins for the functional contribution of Rb1 in Alzheimer's disease (AD). Conclusion: Our proteomic data may provide new insights into the protective mechanisms of Rb1 in AD.

• Journal of Ginseng Research
• /
• v.14 no.2
• /
• pp.191-199
• /
• 1990

It has been well known that extended exposure to reactive oxygens causes severe damage to susceptible biomolecules. In this study, the effects of flavonoids including trifolin and kaempferol from Ginseng leaves on singlet oxygen induced photohemolysis of erythrocytes and free radical scavenging activities were investigated. Each flavonoid aglycone (5-50$\mu$M) such as kaempferol, quercetin or baicalein exhibited a high protective effect against the photohemolysis. They protected the cells by scavenging $^1O_2$ and free radicals Although the free radical scavenging activities of the flavonoid glycosides were not much lower than those of their corresponding aglycones, their insolubility into lipid bilayers of membrane made them less effective in preventing the photohemolysis induced by $^1O_2$. The $^1O_2$ and free radical scavenging activities of flavonoids were estimated by the decomposition of the flavonoid by $^1O_2$ and the bleaching of free radicals by the flavonoid, respectively. The solubilization of the flavonoid into micells or erythrocytes was deduced from spectrophotometric and microscopic observations. The cooperation of L-ascorbic acid and a flavonoid, and a possible involvement of lipoxygenase or cyclooxygenase in the photohemolysis mechanism were discussed.

• Journal of Ginseng Research
• /
• v.42 no.1
• /
• pp.107-115
• /
• 2018

Background: Depression is one of the most commonly diagnosed neuropsychiatric diseases, but the underlying mechanism and medicine are not well-known. Although Panax ginseng has been reported to exert protective effects in various neurological studies, little information is available regarding its antidepressant effects. Methods: Here, we examined the antidepressant effect and underlying mechanism of P. ginseng extract (PGE) in a chronic restraint stress (CRS)-induced depression model in mice. Results: Oral administration of PGE for 14 d decreased immobility (depression-like behaviors) time in forced swim and tail suspended tests after CRS induction, which corresponded with attenuation of the levels of serum adrenocorticotropic hormone and corticosterone, as well as attenuated c-Fos expression in the amygdala. PGE enhanced messenger RNA expression level of brain-derived neurotrophic factor but ameliorated microglial activation and neuroinflammation (the level of messenger RNA and protein expression of cyclooxygenase-2 and inducible nitric oxide synthase) in the amygdala of mice after CRS induction. Interestingly, 14-d treatment with celecoxib, a selective cyclooxygenase-2 inhibitor, and $N_{\omega}$-nitro-L-arginine methyl ester hydrochloride, a selective inducible nitric oxide synthase inhibitor, attenuated depression-like behaviors after CRS induction. Additionally, PGE inhibited the upregulation of the nuclear factor erythroid 2 related factor 2 and heme oxygenase-1 pathways. Conclusion: Taken together, our findings suggest that PGE exerts antidepressant-like effect of CRS-induced depression by antineuroinflammatory and antioxidant (nuclear factor erythroid 2 related factor 2/heme oxygenase-1 activation) activities by inhibiting the hypothalamo-pituitary-adrenal axis mechanism. Further studies are needed to evaluate the potential of components of P. ginseng as an alternative treatment of depression, including clinical trial evaluation.

• Journal of Ginseng Research
• /
• v.28 no.1
• /
• pp.18-26
• /
• 2004

The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract (100 mg kg$^{-1}$ ) was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from 523$\pm$70 to 381$\pm$53 and 120 h post-exercise from 443$\pm$85 to 327$\pm$75 in treated animals. $\beta$-glucuronidase activity, as indicator of inflammation, showed a significant reduction of about 15-25% in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h post-exercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.

• Proceedings of the Ginseng society Conference
• /
• 2002.10a
• /
• pp.159-175
• /
• 2002

The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract $(100\;mg\;kg^{-1})$ was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from $523{\pm}70\;to\;381{\pm}53$ and 120 h post-exercise from $443{\pm}85\;to\;327{\pm}75$ in treated animals. ${\beta}-glucuronidase$ activity, as indicator of inflammation, showed a significant reduction of about $15-25\%$ in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h postexercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.

• Proceedings of the Ginseng society Conference
• /
• 1993.09a
• /
• pp.36-39
• /
• 1993

We reported earlier (Br. J. Pharmac. 82. 485 - 491. 1984) that ginsenosides from Panax ginseng CA. Meyer antagonized noradrenaline or prostaglandin $F_{2\alpha}-induced$ contractions of pulmonary and intrapulmonary arterial rings of rabbits. Because this effect resembled that of acetylcholine (ACh). we questioned whether these acitons were due to release of nitric oxide from vaseular endothelium. We therefore determined whether ginsenosides could vasodilate preconstricted lungs and also protect against free radical injury. which normally eliminates the vasodilator response to ACh(J. Appl. Physiol. 71. 821 - 825. 1991 J. We found that ginsenoside $Rg_1$ or a mixture of saponins could ,a) vasodilate perfused. $U_{46619}-preconstricted$ lungs. b) promote increased synthesis of nitric oxide by endothelial cells in culture and c) prevent the pulmonary edema often associated with free radical injury (Biochem. Biophys. Res. Comm. 189. 670 - 676. 1992). Thus, vasodilator and protective effects of ginsenosides against free radical injury may reflect enhanced synthesis and release of nitric oxide. These data suggest that ginsenosides may be useful in treatment of pulmonary and systemic hypertension. Aided by grants from the National Institutes of Health. Bethesda.

• Proceedings of the Ginseng society Conference
• /
• 1998.06a
• /
• pp.199-207
• /
• 1998

Ginseng saponin (G5) purified from Panax ginseng, increase renal blood flow in rats. Nitric oxide (NO) is thought to be a substance endogenously released by G5 in preconstricted lungs and cultured endothelial cells. The present study aims to determine whether G5 could stimulate endogenous 1'elease of NO in rat kidney and urine levels of the stable NO metabolites, nitrite (NO,) and nitrate (NO,) and urinary COMP levels were measured 8 hr after a single intraperitoneal injection of GS (200 mg/kg) Into rats. The effects of the WO synthesis inhibitor, Nu-nitro-L-arginine methyl ester, .1nd the NO precursor, L-arginine, on the G5-induced changes were also determined. The activity of NO synthase, as determined by conversion of ('"C)-L-arginine to ('"C)-L-citrulline, in whole kidney, glomeruli and cortical tubules were also investigated. A single injection of GS resulted in endogenous production of NO as reflected by increase in serum and urine levels of N021N03 and urinary cGMP levels, which were inhibited by the addition o ( N-nitro-L-arginine methyl ester and restored fly L-arginine. GS also stimulated the activity of NO synthase in whole kidney as well as glomeruli and cortical tubules, and Nu-nitro-L-arginine methyl tilter significantly prevented this increase. In conclusion, GS stimulates endogenous NO production and thus, may play a protective role 1 11 the kidney by modulating renal blood flow.

• Journal of Ginseng Research
• /
• v.38 no.2
• /
• pp.89-96
• /
• 2014

The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue.