• Biomedical Science Letters
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• v.7 no.3
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• pp.127-131
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• 2001

This study was undertaken to examine the effect of amino acids on anoxia-induced cell injury in rabbit renal cortical slices. In order to induce anoxic cell injury, slices were exposed to a 100% $N_2$ atmosphere and control slices were exposed to 100% $O^2$. Irreversible cell injury was estimated by measuring lactate dehydrogenase (LDH) release and alterations in renal cell function were examined by measuring p-aminohippurate (PAH) uptake. Anoxia caused the increase in LDH release in a time-dependent manner. Glycine and glutathione almost completely prevented anoxia-induced LDH release. Of amino acids tested, glycine and alanine exerted the protective effect against anoxia-induced cell injury. However, asparagine with amide side chain, leucine and valine with hydrocarbon side chain, and basic amino acids (lysine, histidine, and arginine) were not effective. Anoxia-induced inhibition of PAM uptake was prevented by glycine. ATP content was decreased by anoxia, which was not affected by glycine. Anoxia-induced depletion of glutathione was significantly prevented by glycine. These results suggest that neutral amino acids with simple structure exert the Protective effect against anoxia-induced cell injury the involvement of specific interaction of amino acids and cell structure.

• Biomedical Science Letters
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• v.10 no.4
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• pp.341-346
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• 2004

Tumor necrosis factor-α (TNF-α) or its mRNA expression are increased in acute nephrosis of various types including ischemia/reperfusion injury. This study was undertaken to determine whether pentoxifylline (PTX), an inhibitor of TNF-α production, provides a protective effect against hypoxia-induced cell injury in rabbit renal cortical slices. To induce hypoxia-induced cell injury, renal cortical slices were exposed to 100% N₂ atmosphere. Control slices were exposed to 100% O₂ atmosphere. The cell injury was estimated by measuring lactate dehydrogenase (LDH) release and p-aminohippurate (PAH) uptake. Exposure of slices to hypoxia increased the LDH release in a time-dependent manner. However, when slices were exposed to hypoxia in the presence of PTX, the LDH release was decreased. The protective effect of PTX was dose-dependent over the concentrations of 0.05∼1 mM. Hypoxia did not increase lipid peroxidation, whereas an organic hydroperoxide t-butylhydroperoxide (tBHP) resulted in a significant increase in lipid peroxidation. PTX did not affect tBHP-induced lipid peroxidation. Hypoxia decreased PAH uptake, which was significantly attenuated by PTX and glycine. tBHP-induced inhibition of PAH uptake was not altered by PTX, although it was prevented by antioxidant deferoxarnine. The PAH uptake by slices in rabbits with ischemic acute renal failure was prevented by PTX pretreatment. These results suggest that PTX may exert a protective effect against hypoxia-induced cell injury and its effect may due to inhibition of the TNF-α production, but not by its antioxidant action.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2613-2617
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• 2015

Radiation induced lung injury has long been considered a treatment limiting factor for patients requiring thoracic radiation. This radiation induced lung injury happens early as well as late. Radiation induced lung injury can occur in two phases viz. early (< 6 months) when it is called radiation pneumonitis and late (>6 months) when it is called radiation induced lung fibrosis. There are multiple factors that can be patient, disease or treatment related that predict the incidence and severity of radiation pneumonitis. Radiation induced damage to the type I pneumocytes is the triggering factor to initiate such reactions. Over the years, radiation therapy has witnessed a paradigm shift in radiation planning and delivery and successfully reduced the incidence of lung injury. Radiation pneumonitis is usually a diagnosis of exclusion. Steroids, ACE inhibitors and pentoxyphylline constitute the cornerstone of therapy. Radiation induced lung fibrosis is another challenging aspect. The pathophysiology of radiation fibrosis includes continuing inflammation and microvascular changes due to pro-angiogenic and profibrogenic stimuli resembling those in adult bronchiectasis. General supportive management, mobilization of airway secretions, anti-inflammatory therapy and management of acute exacerbations remains the treatment option. Radiation induced lung injury is an inevitable accompaniment of thoracic radiation.

• Herbal Formula Science
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• v.9 no.1
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• pp.375-385
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• 2001

Objectives : This study was carried out to research the protective effects of Sagunja-Tang(SA) through in vivo experiments, and tried to investigate the relation between oxidation of liver tissues and deficiency of Qi. Methods : Acute liver injury which initiated from free radical induced by $CCl_4$, were applied to mice and metabolic data were obtained. In order to measure the degree of liver injury, serum level of alanine aminotransferase(AST), aspartate aminotransferase(ALT), creatinine, blood urea nitrogen(BUN), total protein(TP) and glucose were measured. Lipid peroxidation of liver slice was examined by measuring malondialdehyde(MDA), a product of lipid peroxidation. Results : SA had protective effects on $CCl_4$ induced acute liver injury by decreasing serum level of ALT. Kidney injury was induced by injection of $CCl_4$ too, and SA protected kidney injury by decreasing serum level of creatinine and BUN. Conclusions : Through this study, we found that SA have healing effects on liver and kidney injury of $CCl_4$ induced oxidative stress that is similar to deficiency of Qi. And further studies have to be followed to certify the mechanisms.

• The Journal of Internal Korean Medicine
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• v.21 no.2
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• pp.267-274
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• 2000

Objectives : In order to investigate the curative effect of Daesihotang-sosunggitang-gagambang on the liver injury of rats induced by $CCl_4$ and d-galactosamine. Methods : All animals were divided into 5 groups, those were normal group(untreated), control group(administrated with 0.9% Saline solution), sample I group(65mg/kg administrated), sample II group(130mg/kg administrated), positive control group(administrated with 200mg/kg silymarine). After the liver injury of rats induced by ccl4 and d-galactosamine, and cheked the serum transaminase(GOT, GPT) alkaline phosphatase(ALP), lactic dehydrogenase(LDH) for enzyme activities and triglyceride, total cholesterol amounts for serum component were measured. Result : The inhibitory effects on the serum GOT, GPT, LDH, ALP activities, serum total cholesterol content level in liver injury of rats induced by ccl4 were noted in both sample I group and sample II group. The inhibitory effects on the serum GPT, LDH activities and serum total cholesterol content level in liver injury of rats induced by d-galactosamine were noted in both sample I group and sample II group. The inhivitory effects on the serum GOT activities and triglyceride content level in liver injury of rats induced d-galactosamine were noted in sample I group, but it is not recognizable statistically. In sample II, they were noted. Conclusions : Deesihotang-sosoonggitang-gagambang has treatment effect against liver injury in rats induced by ccl4 and d-galactosamine. So it is required to study about the actions of mutual relation of medicines and path-mechanism by experiment.

• Toxicological Research
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• v.32 no.2
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• pp.133-140
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• 2016

Sulfasalzine is a widely administered drug against inflammatory-based disorders in human. However several cases of liver injury are associated with its administration. There is no stabilized safe protective agent against sulfasalazine-induced liver injury. Current investigation was designed to evaluate if N-acetylcysteine (NAC) and dithioteritol (DTT) as thiol reducing agents and/or vitamins C and E as antioxidants have any protective effects against sulfasalazine-induced hepatic injury in an ex vivo model of isolated rat liver. Rat liver was canulated and perfused via portal vein in a closed recirculating system. Different concentrations of sulfasalazine and/or thiol reductants and antioxidants were administered and markers of organ injury were monitored at different time intervals. It was found that 5 mM of sulfasalazine caused marked liver injury as judged by rise in liver perfusate level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) (p < 0.05). A significant amount of lipid peroxidation and hepatic glutathione depletion were detected in drug-treated livers, accompanied with significant histopathological changes of the organ. Administration of NAC ($500{\mu}M$), DTT (${400\mu}M$), Vitamin C ($200{\mu}M$), or vitamin E ($200{\mu}M$) significantly alleviated sulfasalazine-induced hepatic injury in isolated perfused rat liver. The data obtained from current investigation indicate potential therapeutic properties of thiol reductants and antioxidants against sulfasalazine-induced liver injury.

• Biomedical Science Letters
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• v.9 no.4
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• pp.189-193
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• 2003

This study was undertaken to investigate the effect of baicalein, a major flavone component of Scutellaria balicalensis Georgi, on oxidant-induced cell injury in renal epithelial cells. Opossum kidney cells, an established proximal tubular epithelial cells, were used as a cell model of renal epithelial cells and t-butylhydroperoxide (tBHP) as an oxidant drug model. Cell viability was measured by MTT assay and lipid peroxidation was estimated by measuring the content of malondialdehyde, a product of lipid peroxidation. Exposure of cells to tBHP caused cell death and its effect was dose-dependent over concentration range of 0.1~1.0 mM. When cells were exposed to tBHP in the presence of various concentrations (0.1~10 $\mu$M) of baicalein, tBHP-induced cell death was prevented with a manner dependent of baicalein concentration. tBHP induced A TP depletion, which was significantly prevented by baicalein. Similarly, tBHP-induced DNA damage was prevented by baicalein. tBHP produced a marked increase in lipid peroxidation and its effect was completely inhibited by baicalein. These results indue ate that tBHP induces cell injury through a lipid peroxidation-dependent mechanism in renal epithelial cells, and baicalein prevented oxidant-induced cell injury via antioxidant action inhibiting lipid peroxidation. In addition, these results suggest that baicalein may be a candidate for development of drugs which are effective in preventing and treating renal diseases.

• Clinics in Shoulder and Elbow
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• v.10 no.2
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• pp.175-182
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• 2007

Purpose: This study compared the SLAP lesions caused by a sports-induced injury with those caused by a non-sports-induced injury. Materials and Methods: The study was performed on 54 patients who had undergone arthroscopic surgery for a SLAP lesion. There were 21 sports-induced-injury patients (group I) and 36 non-sports-induced injury patients (group II). The mean age of the men was 36 years and that of the women was 48 years. In both groups, the frequency of a concomitant injury and the clinical outcomes at the last follow-up was evaluated using the UCLA score, Rowe score, and the ASES score. Results: According to their injury mechanism, , there were 14 cases (67%) of repeated microtrauma injury in group I and 25 cases (75%) of compression injury type in group II. As a concomitant pathology, there was 11 cases of shoulder instability and 5 cases of a rotator cuff tear in group I, and 23 cases of rotator cuff tears and 14 cases of shoulder instability in group II. At the last follow up, group I showed slightly better clinical satisfaction (P>0.05). Conclusion: The possibility of a SLAP lesion accompanying other diseases is high. Therefore, an accurate assessment of concomitant injury lesions before surgery is important for the treatment outcome.

• Biomedical Science Letters
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• v.8 no.4
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• pp.251-256
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• 2002

This study was undertaken to determine the underlying mechanisms of reactive oxygen species-induced cell injury in renal epithelial cells and whether there is a difference in the role of lipid peroxidation between freshly isolated renal cells and cultured renal cells. Rabbit renal cortical slices were used as a model of freshly isolated cells and opossum kidney (OK) cells as a model of cultured cells. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release in renal cortical slices and frypan blue exclusion in OK cells. $H_2O$$_2$ was used as a drug model of reactive oxygen species. $H_2O$$_2$ induced cell injury in a dose-dependent manner in both cell types. However, renal cortical slices were resistant to $H_2O$$_2$ approximately 50-fold than OK cells. $H_2O$$_2$-induced cell injury was prevented by thiols (glutathione and dithiothreitol) and iron chelators (deferoxamine and phenanthroline) in both cell types. $H_2O$$_2$-induced cell injury in renal cortical slices was completely prevented by antioxidants N,N-diphenyl-p -phenylenediamine and Trolox, but the cell injury was not affected by these antioxidants in OK cells. $H_2O$$_2$ increased lipid peroxidation in both cell types, which was completely inhibited by the antioxidants. These results suggest that $H_2O$$_2$ induces cell injury through a lipid peroxidation-dependent mechanism in freshly isolated renal cells, but via a mechanism independent of lipid peronidation in cultured cells.

• Biomedical Science Letters
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• v.9 no.1
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• pp.37-42
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• 2003

The present study was conducted to determine whether administration of heat extract of Lepidii Semen has an inhibitory effect on neutrophil-derived oxidative injury following dermal scald burn in rats. Acute lung injury was induced by scald burn (15% of TBSA) in rats. To identify acute edematous lung injury, protein concentrations and numbers of polymorphonuclear leukocytes were measured in bronchoalveolar lavage (BAL) at 5 h after skin burn. In addition, the level of lung KC (neutrophil chemoattractant cytokine) and activity of lung myeloperoxidase (MPO) were measured, and histopathological changes were observed as well. Lung weight and concentration of BAL protein, the index of lung injury, were clearly increased at 5 h postburn compared with those of sham-operated group. Administration of heat extract of Lepidii Semen after scald burn inhibited the production of KC in lung tissue and decreased the activity of lung MPO related to infiltration of neutrophils. In histopathological changes in lung tissue, infiltration of inflammatory cells and pulmonary edema induced by skin burn were decreased by administration of heat extract of Lepidii Semen after scald burn. These results suggest that Lepidii Semen may be an effective medical stuff for acute lung injury induced by skin burn.