Effect of Baicalein on t-Butylhydroperoxide-Induced Cell Injury in Renal Tubular Epithelial Cells

Soon-Hee Jung 대한의생명과학회 2003 Biomedical Science Letters Vol.9 No.4

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 цM) of baicalein, tBHP-induced cell death was prevented with a manner dependent of baicalein concentration. tBHP induced ATP 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 inducate 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.

Hydrogen Peroxide-induced Alterations in Na+-phosphate Cotransport in Renal Epithelial Cells

( Soon-hee Jung ) 대한임상검사과학회 2009 대한임상검사과학회지(KJCLS) Vol.41 No.2

This study was undertaken to examine the effect of oxidants on membrane transport function in renal epithelial cells. Hydrogen peroxide (H2O2) was used as a model oxidant and the membrane transport function was evaluated by measuring Na+-dependent phosphate (Na+-Pi) uptake in opossum kidney (OK) cells. H2O2 inhibited Na+-Pi uptake in a dose-dependent manner. The oxidant also caused loss of cell viability in a dose-dependent fashion. However, the extent of inhibition of the uptake was larger than that in cell viability. H2O2 inhibited Na+-dependent uptake without any effect on Na+-independent uptake. H2O2-induced inhibition of Na+-Pi uptake was prevented completely by catalase, dimethylthiourea, and deferoxamine, suggesting involvement of hydroxyl radical generated by an iron-dependent mechanism. In contrast, antioxidants Trolox, N,N’-diphenyl-p-phenylenediamine, and butylated hydroxyanisole did not affect the H2O2 inhibition. Kinetic analysis indicated that H2O2 decreased Vmax of Na+-Pi uptake with no change in the Km value. Phosphonoformic acid binding assay did not show any difference between control and H2O2-treated cells. H2O2 also did not cause degradation of Na+-Pi transporter protein. Reduction in Na+-Pi uptake by H2O2 was associated with ATP depletion and direct inhibition of Na+-K+-ATPase activity. These results indicate that the effect of H2O2 on membrane transport function in OK cells is associated with reduction in functional Na+-pump activity. In addition, the inhibitory effect of H2O2 was not associated with lipid peroxidation.

Ceramide Induces Cell Death through an ERK-dependent Mitochondrial Apoptotic Pathway in Renal Epithelial Cells

( Soon-hee Jung ) 대한임상검사과학회 2010 대한임상검사과학회지(KJCLS) Vol.42 No.1

Ceramide induces cell death in a variety of cell types however, the underlying molecular mechanisms related to renal epithelial cells remain unclear. The present study was undertaken to determine the role of extracellular signal-regulated protein kinase (ERK) in ceramide-induced cell death in renal epithelial cells. An established renal proximal tubular cell line of opossum kidney (OK) cells was used for this research. Ceramide induced apoptotic cell death in these cells. Western blot analysis showed that ceramide induced activation of ERK. The ERK activation and cell death induced by ceramide were prevented by the ERK inhibitor PD98059. Ceramide caused cytochrome C release from mitochondria into the cytosol as well as activation of caspase-3. Both effects were prevented by PD98059. The ceramide-induced cell death was also prevented by a caspase inhibitor. These results suggest that ceramide induces cell death through an ERK-dependent mitochondrial apoptotic pathway in OK cells.

Quercetin Prevents Hydrogen Peroxide-induced Necrotic and Apoptotic Cell Death in Human Colonic Epithelial Cells

( Soon-hee Jung ) 대한임상검사과학회 2011 대한임상검사과학회지(KJCLS) Vol.43 No.4

Quercetin is one of the most distributed flavonoids in the plant kingdom and occurs naturally in a wide range of fruits and vegetables. This study was undertaken to determine whether quercetin exerts beneficial effect against necrotic and apoptotic cell death induced by hydrogen peroxide (H2O2) in intestinal cells using the human-derived cultured T84 colonic epithelial cell line. Necrotic cell death was induced by exposing cells to 0.5 mM H2O2 for 2 h and apoptosis was induced by incubating cells in normal culture medium for 18 h following exposure of cells to 0.5 mM H2O2 for 2 h. Cell viability was evaluated by the trypan blue exclusion assay and apoptosis was assessed by Hoechst 33258 staining and flow cytometry. H2O2 induced necrotic cell death in a time and dose-dependent fashion. Both necrotic and apoptotic cell deaths were not prevented by the antioxidants N,N’-diphenyl-p-phenylenediamine(DPPD) and Trolox, whereas both cell deaths induced by the organic hydroperoxide t-butylhydroperoxide (tBHP) were prevented by DPPD, suggesting that H2O2 induces cell death through a lipid peroxidation-independent mechanism. H2O2-induced necrotic death was prevented by deferoxamine and 3-aminobenzamide, while the apoptotic cell death was not affected by these agents. Quercetin prevented both necrotic and apoptotic cell deaths induced by H2O2 in a dose-dependent manner. H2O2 caused activation of poly (ADP-ribose) polmerase (PARP), which was inhibited by deferoxamine, 3-aminobenzamide, and quercetin, but not DPPD. These results indicate that quercetin inhibits both necroticand apoptotic deaths of T84 cells. The anti-necrotic effect of quercetin may be attributed to its iron chelator activity rather than a direct H2O2 scavenging capacity and antioxidant. The present study suggests that quercetin may play a therapeutic role in the treatment of human gastrointestinal diseases mediated by oxidants.

Diagnostic guideline of malignant mesothelioma in Korea

( Soon Hee Jung ) 대한결핵 및 호흡기학회 2015 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.120 No.-

Beneficial Effect of Pentoxifylline on Hypoxia-Induced Cell Injury in Renal Proximal Tubular Cells

Soon-Hee Jung 대한의생명과학회 2004 Biomedical Science Letters Vol.10 No.4

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-a production, but not by its antioxidant action.

Bronchiolitis Obliterans Organizing Pneumonia: Clinicopathologic Review of a Series of 45 Korean Patients Including Rapidly Progressive form

DongWonKim,SoonheeJung,KibeomLee,JoonChang,JounghoHan,InchulLee,KyoYoungLee,BongKwonChun,BeomJinLim,DongHwanShin,HyeSeungHan,SeongJinCho 대한의학회 2002 Journal of Korean medical science Vol.17 No.2