Protective Effect Of Ginseng Research Articles

Renal Ultrastructural Alterations Induced by Lead Acetate and Protective Effects of Ginseng

Renal Ultrastructural Alterations Induced by Lead Acetate and Protective Effects of Ginseng

Protective effects of ginseng and ginsenosides in the development of osteoarthritis (Review).

Osteoarthritis (OA) is a chronic inflammatory joint disease. Traditional chinese medicine provides a resource for drug screening for OA treatment. Ginseng and the associated bioactive compound, ginsenosides, may reduce inflammation, which is considered a risk factor for the development of OA. Specifically, ginsenosides may exhibit anti-inflammatory and anti-oxidative stress activities, and inhibit extracellular matrix degradation by suppressing the NF-κB and MAPK signaling pathways. Notably, specific ginsenosides, such as compound K and Rk1, may physically interact with IκB kinase and inhibit the associated phosphorylation. Thus, ginsenosides exhibit potential as therapeutic candidates in the management of OA. However, the low water solubility limits the clinical applications of ginsenosides. Numerous effective strategies have been explored to improve bioavailability; however, further investigations are still required.

The protective effects of ginseng on x-irradiation-induced intestinal damage in rats.

Although radiotherapy is widely employed in the treatment of various malignancies in oncology patients, its use is limited by the toxic effects it causes in surrounding tissues, including the gastrointestinal system. Korean Red Ginseng (KRG) is a traditional drug reported to possess antioxidant and restorative properties in various studies. The purpose of the present study was to investigate the protective effects of KRG against radiation-associated small intestinal damage. Twenty-four male Sprague Dawley rats were randomly assigned into three groups. No procedure was performed on Group 1 (control) during the experiment, while Group 2 (x-irradiation) was exposed to radiation only. Group 3 (x-irradiation + ginseng) received ginseng via the intraperitoneal route for a week prior to x-irradiation. The rats were killed 24h after radiation. Small intestinal tissues were evaluated using histochemical and biochemical methods. An increase in malondialdehyde (MDA) levels and a decrease in glutathione (GSH) were observed in the x-irradiation group compared to the control group. KRG caused a decrease in MDA and caspase-3 activity and an increase in GSH. Our findings show that it can prevent damage and apoptotic cell death caused by x-irradiation in intestinal tissue and can therefore play a protective role against intestinal injury in patients receiving radiotherapy.

☆Protective effects of ginseng on memory and learning and prevention of hippocampal oxidative damage in streptozotocin-induced Alzheimer's in a rat model

BackgroundIn the etiology of Alzheimer's disease, the free radicals and Brain cholinergic system function, play a key role. The antioxidant compounds may well be effective in improving this disease. Hence, this study aimed to investigate the effects of ginseng on the treatment and prevention of Alzheimer’s disease in a rat model. Methods56 male Wistar rats were randomly divided into four groups: (1) control, (2) Alzheimer’s without treatment, (3) Alzheimer’s under post-treatment (ginseng, 200 mg/kg/day) for three weeks, and (4) Alzheimer's under pre and post-treatment from one week before induction of Alzheimer's to three weeks after that. To induce Alzheimer's disease 1.5 mg/kg of streptozotocin was injected into both lateral ventricles of the brain. Three weeks after induction, the rats' behavioral tests were applied in all groups. Glutathione peroxidase, Glutathione reductase, Total antioxidant capacity, Malondialdehyde, and Brain-derived neurotrophic factor were measured using commercial kits. Data were analyzed using one-way ANOVA and Bonferroni post hoc test. ResultsLearning and memory, antioxidant defenses, and BDNF showed a significant decrease after the onset of Alzheimer's induction compared with the control group (p < 0.05). Pre and post-treatment of the Alzheimer animals with ginseng significantly improved their learning and memory, antioxidant defenses, and BDNF levels (p < 0.05) compared with the Alzheimer animals without treatment. ConclusionBased on our results, pre and post-treatment with ginseng have protective effects against Alzheimer -induced learning and memory impairment. The effects of ginseng may be mediated through an increase in BDNF and antioxidants levels in the hippocampus region of the brain.

Protective effects of phenolic acid extract from ginseng on vascular endothelial cell injury induced by palmitate via activation of PI3K/Akt/eNOS pathway.

Elevated free fatty acids may impair insulin-mediated signaling to eNOS that contributes to the pathophysiology of endothelial dysfunction. Previous studies have indicated the protective effect of ginseng and the regulatory potential of phenolic acid components from other plants on endothelial function. Therefore, this study investigated the protective effects of phenolic acid extract from ginseng (PG2) on endothelial cells against palmitate-induced damage. We found that PG2 increases cell viability, inhibits the palmitate-induced intracellular accumulation of lipids, and the overexpression of endothelin-1 (ET-1) through enhancing the phosphorylation of the phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase (PI3K/Akt/eNOS) signaling pathway. The results of this study may be valuable for the development of PG2 to combat the endothelial cell damage caused by hyperlipidemia. PRACTICAL APPLICATION: We proved that phenolic acid extract from ginseng has a protective effect on free fatty acid-induced endothelial dysfunction in vitro. This study provides experimental data for the application of ginseng-derived phenolic acids in treating cardiovascular disease.

Protective Effect of Ginseng on Salivary Dysfunction Following Radioiodine Therapy in a Mouse Model.

Following radioiodine (RI) therapy, oxidative stress is a putative damage mechanism resulting in salivary gland (SG) dysfunction. Since ginseng is a known anti-oxidative herb, we examined the SG radioprotective effects of Korea red ginseng (KRG) in a mouse model, when administered prior to RI. Four-week-old mice (n = 60) were divided into four groups: (1) normal control, (2) RI only treated (0.01 mCi/g, orally), (3) KRG administered (0.2 mg/g, intraperitoneal injection) 0.5 and 24 hours before RI, and (4) amifostine-treated group (0.2 mg/g, intraperitoneally) 0.5 hour before RI. The salivary lag times and flow rates were assessed, and sampled tissues were subjected to histologic examinations including hematoxylin and eosin and immunohistochemical staining. Apoptosis was examined by the terminal deoxynucleotidyl transferase biotin-dUDP nick end labeling (TUNEL) assay, and excretion changes in salivary 99mTc pertechnetate were evaluated by single-photon emission computed tomography. The body weight of the KRG group was similar to the control group. Salivary lag times and flow rates in the RI + KRG group were faster than in the RI only group. There was no significant intergroup difference in the SG weight. The RI + KRG group exhibited more mucin-containing parenchyma and less fibrotic tissues than the RI only group. Salivary epithelial (aquaporin 5) and myoepithelial (smooth muscle actin) cells of the RI + KRG group were protected from radiation damage. Low 8-OhdG (oxidative stress biomarker) and high superoxide dismutase 2 (reactive oxygen species scavenger) immunostaining reactivity was detected in the RI + KRG group when compared with the RI only group. Fewer apoptotic cells were observed in the RI + KRG or amifostine group compared to the RI only group in the TUNEL assay. The 99mTc pertechnetate excretion level recovered in the KRG group. Pretreatment with KRG before RI therapy is potentially beneficial in protecting against RI-induced salivary dysfunction.

Abstract TP97: Korean Red Ginseng Ameliorates Cerebral Hypoxic-Ischemic Damage Through the Activation of the Nrf2 Pathway by Preferentially Altering Reactive Astrogliosis

Introduction: Endogenous defense mechanisms by which the brain protects itself against noxious stimuli and recovers from ischemic damage are key targets of stroke research that may ultimately facilitate functional recovery. Multiple evidences indicate that the transcriptional factor Nrf2 plays a vital role in cellular defense against oxidative stress and inflammation, and consequently, targeting Nrf2 has emerged as a promising therapeutic strategy for disease prevention. Korean Red Ginseng (Ginseng), one of the most widely used herbal medicines in the world, has been suggested as one of the most potent Nrf2 activators, thereby making it efficacious against various acute neurological disorders, including stroke. Hypothesis: To evaluate whether Ginseng could exert protective effects against hypoxic-ischemic brain damage and whether Nrf2 activation is pivotal to the various neuroprotective effects of Ginseng. Methods: C57BL/6 WT and Nrf2 knockout mice (10-18 weeks old, n=12-16) were orally administered Ginseng (100mg/kg/d) or vehicle 7d prior to cerebral hypoxic-ischemic damage. At 6 and 24h after stroke, mice were neurologically scored. Brain lesion size and edema formation were measured at 24h. Using immunostaining, we examined which cells appeared to be most preferentially activated in a spatiotemporal pattern by this Nrf2 pathway, in particular, in the early stage of ischemic injury. Based on the results, we are further evaluating the efficacy of inducing the Nrf2 pathway and assess the extended neuroprotective effects of Ginseng at 7d after stroke. Results: Ginseng treatment significantly reduced cerebral infarct size, neuronal death, edema formation and the resultant functional neurological deficits at 24h after stroke (P&lt;0.001); whereas, Nrf2 ablation remarkably attenuated all benefits. Notably, the above protective effects of Ginseng were significantly attenuated in Nrf2 knockouts (P&lt;0.05). In addition, Ginseng treated mice also exhibited reduced neuronal death and delayed severe reactive astrogliosis at 6 and 12h (P&lt;0.05). Conclusion: Our findings indicate a neuroprotective effect of Ginseng against hypoxic-ischemic brain damage, and that Nrf2-dependent cytoprotective responses appear to be more prominent in astrocytes.

A Role of Ginseng and Its Constituents in the Treatment of Central Nervous System Disorders.

Ginseng, a perennial plant belonging to the Panax genus of the Araliaceae family, has been used in China, Korea, and Japan as a traditional herbal medicine for thousands of years. Ginseng is recorded to have exhibited a wide variety of beneficial pharmacological effects and has become a popular and worldwide known health supplement and drug. The protective effects of ginseng on central nervous system are discussed in this review. Ginseng species and ginsenosides and their intestinal metabolism and bioavailability are concisely introduced. The molecular mechanisms of the effects of ginseng on central nervous system, mainly focused on the neuroprotection properties of ginseng, memory, and learning enhanced properties, and the effects on neurodegenerative disorders are presented. Thus, ginseng and its constituents are of potential merits in the treatment of cerebral disorders.

Protective Effects of Processed Ginseng and Its Active Ginsenosides on Cisplatin-Induced Nephrotoxicity: In Vitro and in Vivo Studies.

Although cisplatin can dramatically improve the survival rate in cancer patients, its use is limited by its nephrotoxicity. Previous investigations showed that Panax ginseng contains components that exhibit protective activity against cisplatin-induced nephropathy. The aim of the present study is to investigate the effect of microwave-assisted processing on the protective effect of ginseng and identify ginsenosides that are active against cisplatin-induced kidney damage to evaluate the potential of using ginseng in the management of nephrotoxicity. The LLC-PK1 cell damage by cisplatin was significantly decreased by treatment with microwave-processed ginseng (MG) and ginsenosides Rg3, Rg5, and Rk1. Reduced expression of p53 and c-Jun N-terminal kinase proteins by cisplatin in LLC-PK1 cells was markedly ameliorated after Rg3 and Rg5/Rk1 treatment. Additionally, elevated expression of cleaved caspase-3 was significantly reduced by ginsenosides Rg5, Rk1, and with even greater potency, Rg3. Moreover, MG and its fraction containing active ginsenosides showed protective effects against cisplatin-induced nephropathy in mice. We found that ginsenosides Rg3, Rg5, and Rk1 generated during the heat treatment of ginseng ameliorate renal damage by regulating inflammation and apoptosis. Results of current experiments provide evidence of the renoprotective effects and therapeutic potential of MG and its active ginsenosides, both in vitro and in vivo.

Cisplatin-induced renal toxicity via tumor necrosis factor-α, interleukin 6, tumor suppressor P53, DNA damage, xanthine oxidase, histological changes, oxidative stress and nitric oxide in rats: Protective effect of ginseng

Cisplatin is an effective chemotherapeutic agent successfully used in the treatment of a wide range of solid tumors, while its usage is limited due to its nephrotoxicity. The present study was undertaken to examine the effectiveness of ginseng to ameliorate the renal nephrotoxicity, damage in kidney genomic DNA, tumor necrosis factor-α, interleukin 6, tumor suppressor P53, histological changes and oxidative stress induced by cisplatin in rats. Cisplatin caused renal damage, including DNA fragmentation, upregulates gene expression of tumor suppressor protein p53 and tumor necrosis factor-α and IL-6. Cisplatin increased the levels of kidney TBARS, xanthine oxidase, nitric oxide, serum urea and creatinine. Cisplatin decreased the activities of antioxidant enzymes (GST, GPX, CAT and SOD), ATPase and the levels of GSH. A microscopic examination showed that cisplatin caused kidney damage including vacuolization, severe necrosis and degenerative changes. Ginseng co-treatment with cisplatin reduced its renal damage, oxidative stress, DNA fragmentation and induced DNA repair processes. Also, ginseng diminished p53 activation and improved renal cell apoptosis and nephrotoxicity. It can be concluded that, the protective effects of ginseng against cisplatin induced-renal damage was associated with the attenuation of oxidative stress and the preservation of antioxidant enzymes.

Protective effects of ginseng on neurological disorders.

Ginseng (Order: Apiales, Family: Araliaceae, Genus: Panax) has been used as a traditional herbal medicine for over 2000 years, and is recorded to have antianxiety, antidepressant and cognition enhancing properties. The protective effects of ginseng on neurological disorders are discussed in this review. Ginseng species and ginsenosides, and their intestinal metabolism and bioavailability are briefly introduced. This is followed by molecular mechanisms of effects of ginseng on the brain, including glutamatergic transmission, monoamine transmission, estrogen signaling, nitric oxide (NO) production, the Keap1/Nrf2 adaptive cellular stress pathway, neuronal survival, apoptosis, neural stem cells and neuroregeneration, microglia, astrocytes, oligodendrocytes and cerebral microvessels. The molecular mechanisms of the neuroprotective effects of ginseng in Alzheimer’s disease (AD) including β-amyloid (Aβ) formation, tau hyperphosphorylation and oxidative stress, major depression, stroke, Parkinson’s disease and multiple sclerosis are presented. It is hoped that this discussion will stimulate more studies on the use of ginseng in neurological disorders.

Histological study on the possible protective action of ginseng on the injurious effect induced by acrylamide on the midbrain in adult male albino rat

Introduction Acrylamide is a synthetic chemical compound commonly used in many branches of industry. Researchers have found acrylamide in certain foods that were heated to a temperature above 120°C. Ginseng is a widely used herbal medicine with numerous beneficial effects. Ginseng is suggested to contribute to a protective effect in neurodegenerative disorders. Aim of the study The aim of the present study was to evaluate the possible protective effect of ginseng against the midbrain injury induced by acrylamide in adult male albino rats. Materials and methods A total of 35 adult male albino rats were used. They were divided into three groups. Group I (15 animals) was allowed water ad libitum and fed a standard diet (control). Group II (10 animals) was given acrylamide orally by means of a gastric tube daily at a dose of 30 mg/kg for 4 weeks. Group III (10 animals) was given acrylamide daily at the same dissolution, dose, route and duration as group II concomitantly with ginseng solution through a gastric tube at a dose of 20 mg/kg. Samples from the brainstem were taken and processed for light and electron microscopic investigation. Results Light microscopic examination of the midbrain of the acrylamide-treated animals showed signs of injury. Glial fibrillary acidic protein-positive cells were more abundant in the midbrain of treated animals compared with control animals. Ultrastructural study of the midbrain of the acrylamide-treated group showed dilated RER in association with mitochondria with destroyed cristae. Many myelinated nerve fibers showed degenerative changes. These structural changes were much less pronounced in animals concomitantly treated with acrylamide and ginseng. Conclusion Ginseng can reduce the severity of the injurious effects induced by acrylamide.

Study of Colonic Cell Proliferation Induced by Chronic Toxicity of Orlistat and The Possible Protective Effect of Ginseng in Experimental Animals

Study of Colonic Cell Proliferation Induced by Chronic Toxicity of Orlistat and The Possible Protective Effect of Ginseng in Experimental Animals

DNA Protective Effect of Ginseng and the Antagonistic Effect of Chinese Turnip: A Preliminary Study

The genoprotective effect of American and Asian ginseng on human lymphocytic DNA was studied. Using the comet assay, aqueous extracts of both types of ginseng were shown to diminish hydrogen peroxide-induced DNA damage. In contrast, and in accordance with traditional Chinese medicine beliefs, addition of the juice from Chinese turnip counteracted the beneficial effect of ginseng. Results showed that incubating ginseng along with turnip juice abolished the DNA protective effect of both American and Asian ginseng. Although the exact mechanism has not been elucidated, the counteracting effect of turnip on ginseng seems unlikely to be mediated by enzymatic action as the effect was seen with boiled as well as unboiled turnip extract.

Protective effect of ginseng against acetaminopheninduced renal injury

Protective effect of ginseng against acetaminopheninduced renal injury

Effect of ginseng and prepared aconite injection on TXA2/PGI2 and nuclear factor-κB in rat model of hepatic ischemia-reperfusion

AIM: To explore the protective effects of ginseng and prepared aconite (Shen Fu) injection on the TXA2/PGI2 and nucleus factorκB (NF-κB) in a rat model of hepatic ischemia-reperfusion (IR). METHODS: Twenty-four male Wistar rats weighing 200-250g were randomly divided into Shen Fu (SF) group treated with intraperitoneal SF injection (10 mL/kg) and IR group treated with 0.9% sodium chloride solution (10 mL/kg) as control group. Hepatic ischemia was induced by Pringle s maneuver for 15 minutes, and then reperfusion was performed for one or three hours. Venous blood samples were collected three hours after reperfusion for measurement of TXB2 and 6-keto-PGF(subscript 1α). Liver tissue samples were collected one or three hours after reperfusion, for measurement of deoxidized glutathione (GSH) and morphological and immunochemical studies. RESULTS: Plasma TXB2 was lower in the SF group than in the JR group after three-hour reperfusion (118.7±19.1 vs 386.3±282.7, P＞0.05), while 6-keto-PGF(subscript 1α) was higher in the SF group than in the IR group (1081.7±282.7 vs 960.0±209.9, P＞0.05). The ratio of TXB2 and 6-keto-PGF(subscript 1α) (0.11±0.03 vs 0.39±0.24, P＜0.05) was significantly lower in the SF group. Fifteen minutes after ischemia and one hour after reperfusion, NF-κB p65 was expressed in hepatocytes and Kuffer cells. The percentage of NF-κB p65 positive cells in the SF group was significantly lower (59.33%±11.06% vs 75.83%±11.46%, P＜0.05) and GSH was slightly higher (47.59±19.07 vs 37.32±4.71, P＞0.05) than those in the IR group. Three-hour reperfusion fifteen minutes after ischemia caused important histologic alterations in the liver. Marked structural abnormalities were observed in the IR group, such as massive hepatocyte swelling, necrosis, mitochondria edema and vacuolar changes. In the SF group, hepatic tissue injury was significantly improved. CONCLUSION: Shen Fu injection protects hepatic tissue from ischemia-reperfusion injury by decreasing the ratio of thromboxane A2 and prostacyclin and inhibiting the activation of NF-κB.

Protective Effect of Ginseng on Cytokine-Induced Apoptosis in Pancreatic β-Cells

The effects of ginseng extracts (GE) and several ginsenosides on cytokine-induced apoptosis were evaluated. In pancreatic beta-cell line MIN6N8 cells, the inhibitory effect of GE was significantly observed at 25-100 microg/mL: an 86-100% decrease of cytoplasmic DNA fragments quantified by an ELISA. The inhibitory effect of red ginseng (RG) extract was greater than that of white ginseng (WG) extract (IC50, 3.633 vs 4.942 microg/mL). Screening of several known ginsenosides, which were present in ginseng extracts at 0.124-1.19% (w/w) by HPLC analysis, revealed that the ginsenosides were responsible for the inhibition of beta-cell apoptosis at 0.1-1.0 microg/mL. The molecular mechanism, by which GE inhibited beta-cell apoptosis, appeared to involve the reduction of nitric oxide (NO) and reactive oxygen species (ROS) production, inhibition on p53/p21 expression, and inhibition on cleavage of caspases and poly(ADP-ribose) polymerase (PARP). This study suggests that ginseng may inhibit cytokine-induced apoptosis in beta-cells and, thus, may contribute via this action to the antidiabetic influence in type 1 diabetes.

Protective effect of ginseng against toxic effect of ochratoxin (OA) in kidney of male rats

Protective effect of ginseng against toxic effect of ochratoxin (OA) in kidney of male rats

Protective Effect of Ginseng on Radiation-Induced DNA Double Strand Breaks and Repair in Murine Lymphocytes

We have examined the effects of ginseng on the induction and repair of gamma-ray-induced DNA double strand breaks (dsb) using neutral filter elution technique at pH 9.6 in cultured murine spleen lymphocytes. Ginseng water extract 500 micrograms/ml was added to the culture medium either for 48 hours prior to irradiation. Ginseng extract showed protective effect against the formation of dsb when it was treated for 48 hours before 100 Gy gamma-ray-irradiation. While repair was almost completed until 220.2 minutes after irradiation, DNA repair of irradiated cells in the presence of ginseng extract was did not return to the corresponding control levels even after 621.8 minutes. From these data, it could be calculated that ginseng reduced the relative strand scission factor (RSSF) by about 2. Therefore, it could be concluded that ginseng has radioprotective effect against gamma-ray induced DNA dsb and repair in cultured mouse lymphocytes.