• Archives of Pharmacal Research
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• v.28 no.7
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• pp.791-798
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• 2005

The hepatoprotective activity of flavonol glycosides rich fraction (F-2), prepared from 70% alcohol extract of the aerial parts of V calcarata Desf., was evaluated in a rat model with a liver injury induced by daily oral administration of $CCl_4$ (100 mg/kg, b.w) for four weeks. Treatment of the animals with F-2 using a dose of (25 mg/kg, b.w) during the induction of hepatic damage by $CCl_4$ significantly reduced the indices of liver injuries. The hepatoprotective effects of F-2 significantly reduced the elevated levels of the following serum enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH). The antioxidant activity of F-2 markedly ameliorated the antioxidant parameters including glutathione (GSH) content, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), plasma catalase (CAT) and packed erythrocytes glucose-6-phosphate dehydrogenase (G6PDH) to be comparable with normal control levels. In addition, it normalized liver malondialdehyde (MDA) levels and creatinine concentration. Chromatographic purification of F-2 resulted in the isolation of two flavonol glycosides that rarely occur in the plant kingdom, identified as quercetin-3,5-di-O-$\beta$-D-diglucoside (5) and kaempferol-3,5-di-O-$\beta$-D-diglucoside (4) in addition to the three known compounds identified as quercetin-3-O-$\alpha$-L-rhamnosyl- (${\rightarrow}6$)-$\beta$-D-glucoside [rutin, 3], quercetin-3-O-$\beta$-D-glucoside [isoquercitrin, 2] and kaempferol-3-O-$\beta$-D-glucoside [astragalin, 1]. These compounds were identified based on interpretation of their physical, chemical, and spectral data. Moreover, the spectrophotometric estimation of the flavonoids content revealed that the aerial parts of the plant contain an appreciable amount of flavonoids (0.89%) calculated as rutin. The data obtained from this study revealed that the flavonol glycosides of F-2 protect the rat liver from hepatic damage induced by $CCl_4$ through inhibition of lipid peroxidation caused by $CCl_4$ reactive free radicals.

• Journal of Ginseng Research
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• v.37 no.2
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• pp.187-193
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• 2013

The effect of Korean red ginseng (KRG) on diabetic renal damage was investigated using streptozotocin (STZ)-induced diabetic rats. The diabetic rats showed loss of body weight gain, and increases in kidney weight and urine volume, whereas the oral administration of KRG at a dose of 100 or 250 mg/kg of body weight per day for 28 d prevented these diabetes-induced physiological abnormalities. Among the kidney function parameters, elevated plasma levels of urea nitrogen and creatinine in diabetic control rats tended to be lowered in KRG-treated rats. In addition, administration of KRG at a dose of 100 mg/kg body weight in the diabetic rats showed significant decreases in serum glucose and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), implying that KRG might prevent the pathogenesis of diabetic complications caused by impaired glucose metabolism and oxidative stress. KRG also significantly reduced advanced glycation end product (AGE) formation and secretion from kidney of diabetic rats. Furthermore, KRG decreased the levels of N-(carboxymethyl) lysine and expression of AGE receptor. KRG also reduced the overexpression of cyclooxygenase-2 and inducible nitric oxide synthase in the kidney via deactivation of nuclear factor-kappa B. We also found that KRG prevented STZ-induced destruction of glomerular structure and significantly suppressed high glucose-induced fibronectin production. Taken together, KRG ameliorates abnormalities associated with diabetic nephropathy through suppression of inflammatory pathways activated by TNF-${\alpha}$ and AGEs. These findings indicate that KRG has a beneficial effect on pathological conditions associated with diabetic nephropathy.

• Clinical and Experimental Reproductive Medicine
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• v.48 no.3
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• pp.221-228
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• 2021

Objective: This study investigated the effect of crocin in methylglyoxal (MGO)-induced diabetic male mice. Methods: Seventy 1-month-old male NMRI mice weighing 20-25 g were divided into seven groups (n=10): sham, MGO (600 mg/kg/day), MGO+crocin (15, 30, and 60 mg/kg/day), MGO+metformin (150 mg/kg/day), and crocin (60 mg/kg/day). MGO was administered orally for 30 days. Starting on day 14, after confirming hyperglycemia, metformin and crocin were administered orally. On day 31, plasma and tissue samples were prepared for experimental assessments. Results: Blood glucose and insulin levels in the MGO group were higher than those in the sham group (p<0.001), and decreased in response to metformin (p<0.001) and crocin treatment (not at all doses). Testis width and volume decreased in the MGO mice and improved in the crocin-treated mice (p<0.05), but not in the metformin group. Superoxide dismutase levels decreased in diabetic mice (p<0.05) and malondialdehyde levels increased (p<0.001). Crocin and metformin improved malondialdehyde and superoxide dismutase. Testosterone (p<0.001) and sperm count (p<0.05) decreased in the diabetic mice, and treatment with metformin and crocin recovered these variables. Luteinizing hormone levels increased in diabetic mice (p<0.001) and crocin treatment (but not metformin) attenuated this increase. Seminiferous diameter and height decreased in the diabetic mice and increased in the treatment groups. Vacuoles and ruptures were seen in diabetic testicular tissue, and crocin improved testicular morphology (p<0.01). Conclusion: MGO increased oxidative stress, reduced sex hormones, and induced histological problems in male reproductive organs. Crocin and metformin improved the reproductive damage caused by MGO-induced diabetes.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.1
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• pp.117-125
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• 2007

Neuronal ischemia is a pathological process caused by a lack of oxygen (anoxia) and glucose (hypoglycemia), resulting in neuronal death. It is believed that apoptosis is one of the mechanisms involved in ischemic cell death. Neuronal apoptosis is a process characterized by nuclear DNA fragmentation, changes of plasma membrane organization. To elucidate the mechanism of neuronal death following ischemic insult and to develop neuroprotective effects of Daebowonjeon(DBWJ) against ischemic damage, in vitro models are used. In vitro models of cell death have been devloped with pheochromocytoma (PC12) cell, which have become widely used as neuronal models of oxidative stress, trophic factor, serum deprivation and chemical hypoxia. Using a special ischemic device and PC12 cultures, we investigated an in vitro model of ischemia based on combined Oxygen and Glucose Deprivation (OGD) insult, followed by reoxygenation, mimicking the pathological conditions of ischemia. In this study, Daebowonjeon rescued PC12 cells from Oxygen-Glucose Deprivation (OGD)-induced cell death in a dose-dependent manner The nuclear staining of PC12 cells clearly showed that DBWJ attenuated nuclear condensation and fragmentation which represent typical neuronal apoptotic characteristics. DBWJ also prevents the LDH release and induction of Hypoxia Inducing Factor (HIF)-1 by OGD-exposed PC12 cells. Furthermore, DBWJ reduced the activation of polyADP-ribose polymerase (PARP) by OGO-exposed PC12 cells. These results suggest that apoptosis is an important characteristic of OGD-induced neuronal death and that oriental medicine, such as DBWJ, may prevent PC12 cell from OG D-induced neuronal death by inhibiting the apoptotic process.

• Food Science of Animal Resources
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• v.38 no.2
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• pp.259-272
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• 2018

This study aims to investigate the protective effects of kefir against myocardial infarction induced by isoproterenol (ISO). The rats were randomly divided into 4 groups, each group consisting of 8 rats. The control group, the kefir group (5 mL/kg/d kefir administered to rats as intra-gastric gavage for 60 d), the ISO group (100 mg/kg ISO was administered to rats, s.c. on 61. and 62. d), and kefir+ISO group (5 mL/kg/d kefir was administered to rats intra gastric gavage for 60 days prior to ISO, 100 mg/kg in two doses on day 61 and 62). 12 h after the last ISO dose, all rats were decapitated and their blood samples were collected. Cardiac tissue was reserved for histopathological examination. creatine kinase (CK), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), triglycerides, total cholesterol,very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL) and glucose were measured by autoanalyzer, whole blood malondialdehyde (MDA), glutathione (GSH) and plasma advanced oxidation protein products (AOPP) levels were measured spectrophotometrically. It was determined that in the group of kefir+ISO, the levels of AST (p<0.001), CK (p<0.001), LDH (p<0.001), MDA (p<0.001) and AOPP (p<0.001) were decreased, while the GSH (p<0.05) increased, compared to ISO group. There were no significant changes in lipid profile and glucose levels between these two groups. In conclusion, by examining cardiac enzymes and histopathological changes in cardiac tissue, it can be concluded that the administration of kefir in myocardial infarction induced by ISO can protect the heart with its antioxidant characteristic and minimize the toxic damage created by ISO.

• The Journal of Korean Physical Therapy
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• v.14 no.1
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• pp.63-73
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• 2002

In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total body surface area 30%) except for inhalated injury. At 5 and 24 h after scald burn, biochemical assay in skin tissue, serum and liver tissue were examined. The effects of burn injury on the levels of glutathione, lipid peroxide and on the activities of oxygen of histologic and ultrasound changes, measuring. the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. Post burn 24 h, the content of glutathione was decreased (47.50%), whereas that of lipid peroxide was increased (37.01%), and the activity of superoxide dismutase was diminished (p<0.001). Thus decreasing the capacity of oxygen free radical scavenging enzymes led to oxidative injury in skin tissue. In liver tissue, at 24 h after scald burn, both the content of glutathione and the activity of catalase were markedly decreased (p<0.01, p<0.05), thus the imbalance between free radical generating and scavenging capacities has been induced.

• Nutrition Research and Practice
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• v.8 no.2
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• pp.220-226
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• 2014

BACKGROUND/OBJECTIVES: Arsenic, which causes human carcinogenicity, is ubiquitous in the environment. This study was designed to evaluate modulation of arsenic induced cancer by resveratrol, a phytoalexin found in vegetal dietary sources that has antioxidant and chemopreventive properties, in arsenic trioxide ($As_2O_3$)-induced Male Wistar rats. MATERIALS/METHODS: Adult rats received 3 mg/kg $As_2O_3$ (intravenous injection, iv.) on alternate days for 4 days. Resveratrol (8 mg/kg) was administered (iv.) 1 h before $As_2O_3$ treatment. The plasma and homogenization enzymes associated with oxidative stress of rat kidneys were measured, the kidneys were examined histologically and trace element contents were assessed. RESULTS: Rats treated with $As_2O_3$ had significantly higher oxidative stress and kidney arsenic accumulation; however, pretreatment with resveratrol reversed these changes. In addition, prior to treatment with resveratrol resulted in lower blood urea nitrogen, creatinine and insignificant renal tubular epithelial cell necrosis. Furthermore, the presence of resveratrol preserved the selenium content ($0.805{\pm}0.059{\mu}g/g$) of kidneys in rats treated with $As_2O_3$. However, resveratrol had no effect on zinc level in the kidney relative to $As_2O_3$-treated groups. CONCLUSIONS: Our data show that supplementation with resveratrol alleviated nephrotoxicity by improving antioxidant capacity and arsenic efflux. These findings suggest that resveratrol has the potential to protect against kidney damage in populations exposed to arsenic.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.447-456
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• 2018

Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) ($576{\mu}g/kg/day$) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor ($AT_2R$) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as $TNF-{\alpha}$, MCP-1, $IL-1{\beta}$, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via $AT_2R$.

• The Korea Journal of Herbology
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• v.26 no.3
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• pp.65-73
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• 2011

Objectives : The present study was evaluated the protective roles of Spatholobi Caulis in hepatotoxic rats due to APAP overdose. Methods : In experiments, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE; 50, 100 mg/kg) for 4 days and then, orally gavage with APAP (1.2 g/kg) to induce acute liver damage. Results : Oral injection of APAP caused severe hepatic injury. Plasma ALT, AST and LDH levels were significantly elevated, but SCE significantly decreased ALT, AST and LDH to the normal level. In histopathological analysis, peripheral hemorrhage around portal triads and central necrosis around central veins were founded after APAP treatment. However, these histopathological changes were recovered by SCE pretreatment. SCE also decreased the percentage of generative hepatic regions (%/$mm^2$ hepatic parenchyma), the numbers of inflammatory cells (cells/$mm^2$ hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cellls) which were significantly elevated after APAP injection. Furthermore, SCE down-regulated the contents of hepatic MDA and up-regulated hepatic GSH. SCE also inhibited the decrease in the expression of pro-caspase-3 by APAP treatment. Conclusions : Collectively, these data indicate that SCE protected APAP-induced hapatic damages through antioxidative and anti-apoptotic process. These findings the significant therapeutic potential of SCE during APAP-induced liver injury.

• YAKHAK HOEJI
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• v.51 no.3
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• pp.219-227
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• 2007

Ginsenoside Rgl (Rgl), the pharmacologically active constituent of ginseng (Panax ginseng C.A. Meyer), has a variety of biological activities. The present study was undertaken to evaluate a possibility of Rgl whether it can be used in treatment or prevention of stress disorders. Animals were stressed by immobilization for 2 hours or electroshocks for 20 minutes. The normal group was not exposed to any stress. Rgl was subcutaneously injected as dosages of 5 and 10 mg/kg and red ginseng (RG) was orally administered 200 mg/kg as the positive control. Animals were given supplements for 5 days without stress, and then were given supplements for 5 days with stress. We recorded stress-related behavioral changes of experimental animals using the Etho-vision system. Weight of adrenal gland and levels of corticosterone in plasma were measured and stress related behaviors (smelling, grooming, face washing, rearing) were observed. Rgl didn't make significant behavioral changes in total open field and elevated plus maze test. Rgl did not influence on behavioral changes induced by electroshock stress. Whereas, 10 mg/kg of Rgl alleviated the increment of the freezing and face washing time and the decrement of the smelling and rearing time induced by restraint stress. The administration of Rgl 10 mg/kg has significantly increased the endurance time on rotating rod and swimming pool tests compared to the control group. These results indicate that Rgl can alleviate the damage induced by physical stress. This result suggests that Rgl may bea new candidate for treating stress related disorder.