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Oh, Gi-Su,Kim, Hyung-Jin,Choi, Jae-Hyuck,Shen, AiHua,Choe, Seong-Kyu,Karna, Anzani,Lee, Seung Hoon,Jo, Hyang-Jeong,Yang, Sei-Hoon,Kwak, Tae Hwan,Lee, Chul-Ho,Park, Raekil,So, Hong-Seob Springer-Verlag 2014 Kidney international Vol.85 No.3
Cisplatin is a widely used chemotherapeutic agent for the treatment of various tumors. In addition to its antitumor activity, cisplatin affects normal cells and may induce adverse effects, such as ototoxicity, nephrotoxicity, and neuropathy. Various mechanisms, such as DNA adduct formation, mitochondrial dysfunction, oxidative stress, and inflammatory responses, are critically involved in cisplatin-induced adverse effects. As NAD<SUP>+</SUP> is a cofactor for various enzymes associated with cellular homeostasis, we studied the effects of increased NAD<SUP>+</SUP> levels by means of NAD(P)H:quinone oxidoreductase 1 (NQO1) activation using a known pharmacological activator (β-lapachone) in wild-type and NQO1<SUP>−/−</SUP> mice on cisplatin-induced renal dysfunction in vivo. The intracellular NAD<SUP>+</SUP>/NADH ratio in renal tissues was significantly increased in wild-type mice co-treated with cisplatin and β-lapachone compared with the ratio in mice treated with cisplatin alone. Inflammatory cytokines and biochemical markers for renal damage were significantly attenuated by β-lapachone co-treatment compared with those in the cisplatin alone group. Notably, the protective effects of β-lapachone in wild-type mice were completely abrogated in NQO1<SUP>−/−</SUP> mice. Moreover, β-lapachone enhanced the tumoricidal action of cisplatin in a xenograft tumor model. Thus, intracellular regulation of NAD<SUP>+</SUP> levels through NQO1 activation might be a promising therapeutic target for the protection of cisplatin-induced acute kidney injury.
Review : Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies
( Gi Su Oh ),( Hyung Jin Kim ),( Ai Hua Shen ),( Su Bin Lee ),( Dipendra Khadka ),( Arpana Pandit ),( Hong Seob So ) 대한전해질학회 2014 Electrolytes & Blood Pressure Vol.12 No.2
Cisplatin is one of the most widely used and highly effective drug for the treatment of various solid tumors; however, it has dose-dependent side effects on the kidney, cochlear, and nerves. Nephrotoxicity is the most well-known and clinically important toxicity. Numerous studies have demonstrated that several mechanisms, including oxidative stress, DNA damage, and inflammatory res-ponses, are closely associated with cisplatin-induced nephrotoxicity. Even though the establishment of cisplatin-induced nephrotoxicity can be alleviated by diuretics and pre-hydration of patients, the prevalence of cisplatin nephrotoxi- city is still high, occurring in approximately one-third of patients who have under- gone cisplatin therapy. Therefore it is imperative to develop treatments that will ameliorate cisplatin-nephrotoxicity. In this review, we discuss the mechanisms of cisplatin-induced renal toxicity and the new strategies for protecting the kidneys from the toxic effects without lowering the tumoricidal activity.
( Gi-su Oh ),( Su-bin Lee ),( Anjani Karna ),( Hyung-jin Kim ),( Aihua Shen ),( Arpana Pandit ),( Seunghoon Lee ),( Sei-hoon Yang ),( Hong-seob So ) 대한결핵 및 호흡기학회 2016 Tuberculosis and Respiratory Diseases Vol.79 No.4
Background: Idiopathic pulmonary fibrosis is a common interstitial lung disease; it is a chronic, progressive, and fatal lung disease of unknown etiology. Over the last two decades, knowledge about the underlying mechanisms of pulmonary fibrosis has improved markedly and facilitated the identification of potential targets for novel therapies. However, despite the large number of antifibrotic drugs being described in experimental pre-clinical studies, the translation of these findings into clinical practices has not been accomplished yet. NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to NAD<sup>+</sup> by various quinones and thereby elevates the intracellular NAD+ levels. In this study, we examined the effect of increase in cellular NAD<sup>+</sup> levels on bleomycin-induced lung fibrosis in mice. Methods: C57BL/6 mice were treated with intratracheal instillation of bleomycin. The mice were orally administered with モ-lapachone from 3 days before exposure to bleomycin to 1-3 weeks after exposure to bleomycin. Bronchoalveolar lavage fluid (BALF) was collected for analyzing the infiltration of immune cells. In vitro, A549 cells were treated with transforming growth factor β1 (TGF-β1) and モ-lapachone to analyze the extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT). Results: β-Lapachone strongly attenuated bleomycin-induced lung inflammation and fibrosis, characterized by histological staining, infiltrated immune cells in BALF, inflammatory cytokines, fibrotic score, and TGF-β1, α-smooth muscle actin accumulation. In addition, β-lapachone showed a protective role in TGF-β1-induced ECM expression and EMT in A549 cells. Conclusion: Our results suggest that β-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-β1-induced EMT in vitro, by elevating the NAD<sup>+</sup>/NADH ratio through NQO1 activation.
Oh, Gi-Su,Lee, Su-Bin,Karna, Anjani,Kim, Hyung-Jin,Shen, AiHua,Pandit, Arpana,Lee, SeungHoon,Yang, Sei-Hoon,So, Hong-Seob The Korean Academy of Tuberculosis and Respiratory 2016 Tuberculosis and Respiratory Diseases Vol.79 No.4
Background: Idiopathic pulmonary fibrosis is a common interstitial lung disease; it is a chronic, progressive, and fatal lung disease of unknown etiology. Over the last two decades, knowledge about the underlying mechanisms of pulmonary fibrosis has improved markedly and facilitated the identification of potential targets for novel therapies. However, despite the large number of antifibrotic drugs being described in experimental pre-clinical studies, the translation of these findings into clinical practices has not been accomplished yet. NADH:quinone oxidoreductase 1 (NQO1) is a homodimeric enzyme that catalyzes the oxidation of NADH to $NAD^+$ by various quinones and thereby elevates the intracellular $NAD^+$ levels. In this study, we examined the effect of increase in cellular $NAD^+$ levels on bleomycin-induced lung fibrosis in mice. Methods: C57BL/6 mice were treated with intratracheal instillation of bleomycin. The mice were orally administered with ${\beta}$-lapachone from 3 days before exposure to bleomycin to 1-3 weeks after exposure to bleomycin. Bronchoalveolar lavage fluid (BALF) was collected for analyzing the infiltration of immune cells. In vitro, A549 cells were treated with transforming growth factor ${\beta}1$ (TGF-${\beta}1$) and ${\beta}$-lapachone to analyze the extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT). Results: ${\beta}$-Lapachone strongly attenuated bleomycin-induced lung inflammation and fibrosis, characterized by histological staining, infiltrated immune cells in BALF, inflammatory cytokines, fibrotic score, and TGF-${\beta}1$, ${\alpha}$-smooth muscle actin accumulation. In addition, ${\beta}$-lapachone showed a protective role in TGF-${\beta}1$-induced ECM expression and EMT in A549 cells. Conclusion: Our results suggest that ${\beta}$-lapachone can protect against bleomycin-induced lung inflammation and fibrosis in mice and TGF-${\beta}1$-induced EMT in vitro, by elevating the $NAD^+$/NADH ratio through NQO1 activation.
Oh, Gi-Su,Pae, Hyun-Ock,Choi, Byung-Min,Kwon, Ji-Wung,Yun, Yeong-Ho,Choi, Jeong-Ho,Kwon, Tae-Oh,Park, Young-Chul,Chung, Hun-Teag The Korean Association of Immunobiologists 2003 Immune Network Vol.3 No.3
Background: The mushroom Phellinus linteus (PL) has been shown to have the anti-tumor and immunostimulatory effects. We hypothesized that the hot water extract of PL (WEPL) exerts its significant immunostimulatory effect by inducing production of the Th1-derived cytokine interferon-${\gamma}$ (IFN-${\gamma}$) by T lymphocytes. Methods: T lymphocytes were isolated from the mice fed with 200 mg/kg of WEPL once a day for 4 weeks, and then stimulated with the mitogen concanavaline A (Con A). IFN-${\gamma}$ gene and intracellular protein expressions were analyzed by RT-PCR and flow cytometry, respectively. The production of IFN-${\gamma}$ was measured by enzyme-linked immunosorbent assay. Results: WEPL significantly enhanced the transcription of IFN-${\gamma}$ mRNA. The effect of WEPL on IFN-${\gamma}$ expression was further supported by a concomitant increase in the number of cells with intracellular IFN-${\gamma}$ protein as well as the secretion of IFN-${\gamma}$. However, WEPL did not modulate either gene expression or protein secretion of interleukin-4, a Th2-associated cytokine, by Con A-stimulated T lymphocytes. Conclusion: Our results demonstrate that one of the potentially beneficial anti-tumor and immunostimulatory effects of WEPL may be mediated through the enhancement of IFN-${\gamma}$ secretion by T lymphocytes.
Deep Neck Space Infection Caused by Keratocystic Odontogenic Tumor
Oh, Ji-Su,Kim, Su-Gwan,You, Jae-Seek,Min, Hong-Gi,Kim, Ji-Won,Kim, Eun-Sik,Kim, Cheol-Man,Lim, Kyung-Seop Korean Association of Maxillofacial Plastic and Re 2014 Maxillofacial Plastic Reconstructive Surgery Vol.36 No.2
Keratocystic odontogenic tumor (KCOT) is a benign cystic intraosseous tumor of odontogenic origin. An infection of a KCOT is not common because KCOT is a benign developmental neoplasm. Moreover, a severe deep neck space infection with compromised airway caused by infected KCOT is rare. This report presents a 60-year-old male patient with a severe deep neck space infection related to an infected KCOT due to cortical bone perforation and rupture of the exudate. Treatment of the deep neck space infection and KCOT are reported.
New Therapeutic Concept of NAD Redox Balance for Cisplatin Nephrotoxicity
Oh, Gi-Su,Kim, Hyung-Jin,Shen, AiHua,Lee, Su-Bin,Yang, Sei-Hoon,Shim, Hyeok,Cho, Eun-Young,Kwon, Kang-Beom,Kwak, Tae Hwan,So, Hong-Seob Hindawi Publishing Corporation 2016 BioMed research international Vol.2016 No.-
<P>Cisplatin is a widely used chemotherapeutic agent for the treatment of various tumors. In addition to its antitumor activity, cisplatin affects normal cells and may induce adverse effects such as ototoxicity, nephrotoxicity, and peripheral neuropathy. Various mechanisms such as DNA adduct formation, mitochondrial dysfunction, oxidative stress, and inflammatory responses are closely associated with cisplatin-induced nephrotoxicity; however, the precise mechanism remains unclear. The cofactor nicotinamide adenine dinucleotide (NAD<SUP>+</SUP>) has emerged as a key regulator of cellular energy metabolism and homeostasis. Recent studies have demonstrated associations between disturbance in intracellular NAD<SUP>+</SUP> levels and clinical progression of various diseases through the production of reactive oxygen species and inflammation. Furthermore, we demonstrated that reduction of the intracellular NAD<SUP>+</SUP>/NADH ratio is critically involved in cisplatin-induced kidney damage through inflammation and oxidative stress and that increase of the cellular NAD<SUP>+</SUP>/NADH ratio suppresses cisplatin-induced kidney damage by modulation of potential damage mediators such as oxidative stress and inflammatory responses. In this review, we describe the role of NAD<SUP>+</SUP> metabolism in cisplatin-induced nephrotoxicity and discuss a potential strategy for the prevention or treatment of cisplatin-induced adverse effects with a particular focus on NAD<SUP>+</SUP>-dependent cellular pathways.</P>
( Gi-ae Kim ),( Han Hee Lee ),( Su Jin Jeong ),( Jin San Lee ),( Key-Chung Park ),( In-hwan Oh ),( Jae-jun Shim ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Fatty liver disease and dementia are emerging health problems in many countries. Hepatic steatosis is a feature of abnormal fat metabolism in the body. Fat dysregulation in the brain might also increase risk for dementia. The aim of this study was to investigate whether hepatic steatosis is associated with development of dementia in the middle-aged population. Methods: A nationwide population-based cohort study was conducted using customized data from the National Health Insurance Service of Korea. We identified subjects (40 to 69 years) who conducted two or more health examinations between 2004 and 2007, who were free of chronic viral hepatitis, alcoholic liver disease, cirrhosis, cancers, stroke, and dementia. Fatty liver was defined using hepatis steatosis index (HSI) > 36. Control was defined when all HSIs were less than 30 between 2004 and 2007. Dementia was identified using disease classification codes (F00, F01, F02, F03, G30, G31, or G32) and prescription data of an antidementia drug. Enrolled subjects (n=3,811,942) were observed until 2017 and incidence of dementia was evaluated according to fatty liver. Results: Among the control group (all HSI < 30, n=651,481), dementia was identified in 37,182 persons (5.4%) during follow-up (2007 - 2017). Among subjects with all HSI > 36 (n=439,654), dementia was identified in 36,093 persons (7.59%, P< 0.0001). After adjusting for sex, age, liver enzymes, body mass index, smoking status, diabetes, hypertension, cholesterol, and disability, the multivariate analysis showed non-alcoholic fatty liver (any HSI > 36) was significantly associated with incidence of dementia (adjusted HR 1.08; 95% CI 1.06- 1.10). In subgroup analysis, dementia was not associated with improved fatty liver (initial HSI > 36, last HSI < 30), (adjusted HR 1.05; 95% CI 0.99-1.11). However, aggravated fatty liver (initial HSI < 30, last HSI > 36) was significantly associated with dementia (adjusted HR 1.10; 95% CI 1.03-1.17). Sustained fatty liver (all HSI > 36) was also associated with dementia (adjusted HR 1.03; 95% CI 1.01-1.16). Conclusions: Non-alcoholic fatty liver is associated with development of dementia in middle-aged Korean population.