• Advances in Traditional Medicine
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• 제9권4호
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• pp.292-302
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• 2009

Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies showed that antioxidant treatments attenuated renal ischemia/reperfusion injury. The objective of this study was to examine the role of hesperidin in modulating reactive oxygen species induced inflammation and apoptosis after renal ischemia/reperfusion injury. Rats were subjected to right nephrectomy, 15 days later 45 min of renal ischemia and 24 h reperfusion with or without treatment with hesperidin. Renal function, inflammation and apoptosis were compared at 24 h after reperfusion injury. Hesperidin improved the renal dysfunction and reduced inflammation and apoptosis after ischemia/reperfusion injury. In conclusion, hesperidin shows potent anti-apoptotic and antiinflammatory properties due to antioxidant property. These findings may have major implications in the treatment of human ischemic acute renal failure.

• IMMUNE NETWORK
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• 제1권3호
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• pp.213-220
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• 2001

Background: A previous study has shown that Euonymus alatus (EA) has an antidotic activities against inflammation, suggesting possibility that EA can exert this beneficial effects to liver injury by an initial protection against drug-induced hepatocyte demage. The present study was undertaken to evaluate the protective effect of EA-extract on experimentally induced hepatitis in ICR mice and to investigate some mechanisms responsible for its action. Methods: Water EA extract was used in this experiments. The mice received i.p. a dose of 700 mg/kg galactosamine (GalN) together with $5{\mu}g/kg$ of endotoxin (LPS), or received i.v. 12 mg/kg of concanavalin A (Con A). EA (4 mg/mouse) was administrated on day -2, -1 and 0 before induction of liver injury. Liver injury was assessed by measurement of serum alanin amino-transferase (SGPT) levels on 9 hr after GaIN.LPS, or 8 hr after con A administration. Results: Treatment with either GaIN or LPS alone did not cause hepatitis. However, simultaneous administration of GalN and LPS to mice resulted in LPS-dose dependent fulminant hepatitis. GaLN/LPS-induced liver injury was reduced when mice were given EA for 3 days before induction. This preventive effect of Ea was more prominent when EA was given by intraperitoneal route rather then by oral route. Pretreatment of EA or dexamethasone inhibited significantly $TNF{\alpha}$ production in GalL/LPS-injured mice. However, EA-treatment did not influence $TNF{\alpha}$-induced hepatitis in GalN-sensitized mice, suggesting that $TNF{\alpha}$ is likely to act as one of final mediators of endotoxin action and the protective effect of EA might be manifested chiefly by inhibition of endotoxin-induced $TNF{\alpha}$ production, not by blocking the $TNF{\alpha}$-action. Injection of Con A into mice evoked remarkable liver injury in a dose dependent fashion. This liver damage was reduced by EA-pretreatment. Dexamethasone significantly reduced both GalL/LPS-induced and Con A-induced liver damages, showing synergism with EA. However, indomethacin reduced only GalN/ LPS-induced hepatitis, not for Con A-induced hepatitis. Conclusion: These results led to the conclusion that EA may be able to contribute at least in part to prevent the drug-induced hepatotoxicity, and that its anti-hepatitis effects might be manifested directly by modulation of endogenous mediators, such as leukotriese D4, $TNF{\alpha}$ and free radical, and indirectly by regulation of immune mediated responses. Also these results suggested that EA could be developed as a potential antidotic agent.

• Korean Journal of Acupuncture
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• 제27권1호
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• pp.49-62
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• 2010

Objective: This study was performed to investigate the effect of manual acupuncture, invasive laser acupuncture and laser skin irradiation at LU8, LR4, HT8 and LR2(Liver Seunggyeok) on D-galN-induced liver injury in rats. Method: Liver injury was induced with D-galN. The experimental rats were divided four groups(Control group, EXP-1, EXP-2, EXP-3). In the Control group, liver injury-induced and not treated. EXP-1 group was liver injury-induced and carried out manual acupuncture with Young-Su(against the meridian course and following the course of the meridian) & Won-Bang(by twisting and rotating the needle) acupuncture method at Liver Seunggyeok. EXP-2 group was liver injury-induced and carried out invasive laser acupuncture at Liver Seunggyeok. EXP-3 group was liver injury-induced and carried out laser skin irradiation at Liver Seunggyeok. Result: In the change of body weight(in 1 week), EXP-1, EXP-2 and EXP-3 groups were significantly increased as compared with control group. In the change AST & ALT, EXP-1 and EXP-2 groups were significantly decreased as compared with control group. In the change of SOD, EXP-1, EXP-2 and EXP-3 groups were significantly increased as compared with control group. In the change of WBC, EXP-2 group was significantly increased as compared with control group. Conclusion: Manual acupuncture, invasive laser acupuncture and laser skin irradiation at Liver Seunggyeok had hepatotherapeutic effect on the treatment of hepatocytotoxity. Invasive laser acupuncture was as effective as manual acupuncture on the treatment of hepatocytotocity.

• BMB Reports
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• 제53권6호
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• pp.311-316
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• 2020

Cholestasis is a condition in which the bile duct becomes narrowed or clogged by a variety of factors and bile acid is not released smoothly. Bile acid-induced liver injury is facilitated by necrotic cell death, neutrophil infiltration, and inflammation. Metformin, the first-line treatment for type 2 diabetes, is known to reduce not only blood glucose but also inflammatory responses. In this study, we investigated the effects of metformin on liver injury caused by cholestasis with bile acid-induced hepatocyte injury. Static bile acid-induced liver injury is thought to be related to endoplasmic reticulum (ER) stress, inflammatory response, and chemokine expression. Metformin treatment reduced liver injury caused by bile acid, and it suppressed ER stress, inflammation, chemokine expression, and neutrophil infiltration. Similar results were obtained in mouse primary hepatocytes exposed to bile acid. Hepatocytes treated with tauroursodeoxycholic acid, an ER stress inhibitor, showed inhibition of ER stress, as well as reduced levels of inflammation and cell death. These results suggest that metformin may protect against liver injury by suppressing ER stress and inflammation and reducing chemokine expression.

• Journal of Microbiology and Biotechnology
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• 제31권8호
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• pp.1069-1078
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• 2021

Sevoflurane postconditioning (SPostC) has been proved effective in cardioprotection against myocardial ischemia/reperfusion injury. It was also reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. However, the mechanism by which sevoflurane protects cardiomyocytes via HSP70 is still not understood. Here, we aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes. After the HR cardiomyocytes model was established, the cells transfected with siRNA for HSP70 (siHSP70) or not were treated with sevoflurane during reoxygenation. The lactate dehydrogenase (LDH) level was detected by colorimetry while cell viability and apoptosis were detected by MTT and flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect HSP70, apoptosis-, cell cycle-associated factors, iNOS, and Cox-2 expressions. Enzyme-linked immuno sorbent assay (ELISA) was used to measure malondialdehyde (MDA) and superoxide dismutase (SOD). SPostC decreased apoptosis, cell injury, oxidative stress and inflammation and increased viability of HR-induced cardiomyocytes. In addition, SPostC downregulated Bax and cleaved caspase-3 levels, while SPostC upregulated Bcl-2, CDK-4, Cyclin D1, and HSP70 levels. SiHSP70 had the opposite effect that SPostC had on HR-induced cardiomyocytes. Moreover, siHSP70 further reversed the effect of SPostC on apoptosis, cell injury, oxidative stress, inflammation, viability and the expressions of HSP70, apoptosis-, and cell cycle-associated factors in HR-induced cardiomyocytes. In conclusion, this study demonstrates that SPostC can reduce the HR injury of cardiomyocytes by inducing HSP70 expression.

• 대한한의학회지
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• 제27권4호
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• pp.156-161
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• 2006

Object : Warming acupuncture (WA) has been used in Oriental Medicine for the treatment of physical disabilities caused by ligament damage. Here, the effects of WA on injured ligament tissues were investigated using the rat model. Methods : The rats were induced injury on the right hind ankle, and 4 weeks later, WA was given onto the acupoint GB4O(Quixu) of the injury area on a weekly basis for 6 weeks. Main outcome was measured by levels of Erk1/2. Hoechst nuclear staining and collagen staining in the ligament tissue. Result : Levels of active form of Erk1/2 kinase were increased in the injured ligament with WA compared with the control ligament induced injury only, and this change correlated with cell number increases in the ligament by WA. Type III, but not type I, collagen mRNA and protein levels were elevated in the injured ligament treated with WA. Moreover, histological staining showed increased re-organization of collagen fibers in the ligament by WA. Conclusions : The present data suggest that WA performance to the injured ligament may facilitate the healing process via increasing cellular activity.

• Radiation Oncology Journal
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• 제32권3호
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• pp.103-115
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• 2014

To summarize current knowledge regarding mechanisms of radiation-induced normal tissue injury and medical countermeasures available to reduce its severity. Advances in radiation delivery using megavoltage and intensity-modulated radiation therapy have permitted delivery of higher doses of radiation to well-defined tumor target tissues. Injury to critical normal tissues and organs, however, poses substantial risks in the curative treatment of cancers, especially when radiation is administered in combination with chemotherapy. The principal pathogenesis is initiated by depletion of tissue stem cells and progenitor cells and damage to vascular endothelial microvessels. Emerging concepts of radiation-induced normal tissue toxicity suggest that the recovery and repopulation of stromal stem cells remain chronically impaired by long-lived free radicals, reactive oxygen species, and pro-inflammatory cytokines/chemokines resulting in progressive damage after radiation exposure. Better understanding the mechanisms mediating interactions among excessive generation of reactive oxygen species, production of pro-inflammatory cytokines and activated macrophages, and role of bone marrow-derived progenitor and stem cells may provide novel insight on the pathogenesis of radiation-induced injury of tissues. Further understanding the molecular signaling pathways of cytokines and chemokines would reveal novel targets for protecting or mitigating radiation injury of tissues and organs.

• BMB Reports
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• 제38권5호
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• pp.563-570
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• 2005

Tamoxifen citrate (TAM), is widely used for treatment of breast cancer. It showed a degree of hepatic carcinogenesis. The purpose of this study was to elucidate the antioxidant capacity of green tea (Camellia sinensis) extract (GTE) against TAM-induced liver injury. A model of liver injury in female rats was done by intraperitoneal injection of TAM in a dose of $45\;mg\;Kg^{-1}\;day^{-1}$, i.p. for 7 successive days. GTE in the concentration of 1.5%, was orally administered 4 days prior and 14 days after TAM-intoxication as a sole source of drinking water. The antioxidant flavonoid; epicatechin (a component of green tea) was not detectable in liver and blood of rats in either normal control or TAM-intoxicated group, however, TAM intoxication resulted in a significant decrease of its level in liver homogenate of tamoxifen-intoxicated rats. The model of TAM-intoxication elicited significant declines in the antioxidant enzymes (glutathione-S-transferase,glutathione peroxidase, superoxide dismutase and catalase) and reduced glutathione concomitant with significant elevations transaminase) levels. The oral administration of 1.5% GTE to TAM-intoxicated rats, produced significant increments in the antioxidant enzymes and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases levels. The data obtained from this study speculated that 1.5% GTE has the capacity to scavenge free radical and can protect against oxidative stress induced by TAM intoxication. Supplementation of GTE could be useful in alleviating tamoxifen-induced liver injury in rats.

• 대한한방내과학회지
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• 제25권3호
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• pp.539-544
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• 2004

Herbal medicine has been used in the Eastern world for 2,000 years, and is beneficial for numerous diseases. There have been reports pertaining to the safety of herbal medicine, but there have been few reports about herbal medicine induced liver injury in Eastern or Western medicine. Most are descriptions of hepatotoxicity of certain toxic herbs. We experienced one case of drug induced liver injury in the treatment of cerebral infarction with Chungsim Yeonja-tang. Although the patient had not used medication and Chungsim Yeonja-tang has no toxic herbs in it. patient's ALP, AST, ALT, GGT was twice elevated after 20 days on medication. This was diagnosed as drug induced liver injury, possibly due to incorrect diagnosis of Sasang constitution. So no herbal medicine was given for seven days. Then Gagam Saeng Gan-tang was given. Gagam Saeng Gan-tang have been used to treat hepatic disease and have been known to have beneficial effects. After 25 days on medication, the clinical symptoms and liver function improved. So, this case is presented to bring more attention to the toxicity of herbal medicines.

• 대한본초학회지
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• 제21권3호
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• pp.69-74
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• 2006

Objectives : This study was undertaken to determine if a combined(SPe) has a protective effect against functional failure induced by $CCl_4$ in rat liver. Methods : Acute liver injury which initiated from free radical induced by $CCl_4$, were applied to rats and data were obtained. Liver injury was estimated by measuring aspartate aminotransferase(AST) and alanine aminotransferase(ALT) activity in serum. Lipid peroxidation was examined by measuring malondialdehyde, a product of lipid peroxidation. GSH activities in liver tissues were also measured. Results : When rats were treated intraperitoneally with $CCl_4$, serum AST and ALT were increased compared with the control, which was significantly inhibited by pretreatment of SPe. SPe also prevented reduction in GSH induced by $CCl_4$. Conclusion : Above results suggest that SPe exerts protective effect against $CCl_4$ by its antioxidant action in liver tissues. Thus, SPe may be used in prevention and treatment of drug-induced liver cell injury. However, the precise mechanisms of SPe protection remain to be determined.