10 research outputs found
μ€λ°°μ λ° λ΄μΆ μΆμΆλ¬Όμ νΌλΆ λ Ένμ νΌλΆμμ λν μμ© λ©μ»€λμ¦μ λΆμμ μ°κ΅¬
νμλ
Όλ¬Έ(λ°μ¬) -- μμΈλνκ΅λνμ : λμ
μλͺ
κ³Όνλν λμλͺ
곡νλΆ, 2021.8. μ₯νμ.κ³Όλν μμΈμ (UV)μ λ
ΈμΆμ νΌλΆ μΌμ¦ λ° νΌλΆμ λ°μμ μ£Όμ μμΈ μ€ νλμ΄λ€. μ μ μ μμΈκ³Ό μνμ΅κ΄μ λ°λΌ κ·Έ κ²½ν₯μ λ€λ₯΄κ² λνλ μ μμ§λ§, λ°λ³΅μ μΌλ‘ μμΈμ μ λ
ΈμΆλ νΌλΆλ λΆκ·μΉν κ°μ λ°μ κ³Ό μ£Όλ¦ νμ±μ΄ λνλλ©°, μ΄λ₯Ό μ΄μΉνμ¬ κ΄λ
Έν(photoaging)λΌκ³ νλ€. μ μ¬ μΈμ AP-1μ mmp-1κ³Ό cox-2 μ μ μμ λ°ν μ‘°μ μ ν΅ν΄ κ΄λ
Έν, νΌλΆμΌμ¦, νΌλΆμμ λ°μμ μ£Όμν μν μ νλ€. AP-1μ΄ μμΈμ μ μν κ΄λ
Έν λ° μΌμ¦μ μ€μ¬ 맀κ°μ²΄μ΄κΈ° λλ¬Έμ, AP-1 νμ±μ μ΅μ ν μ μλ νν©λ¬Όμ ν¨μ¨μ μΌλ‘ μ λ³ κ°λ₯ν λΆμ λꡬμ κ°λ°μ μλ‘μ΄ ν κ΄λ
Έν λ° ν μΌμ¦ μ λ₯Ό κ°λ°νκΈ° μν ν¨κ³Όμ μΈ μ λ΅μ΄ λ κ²μ΄λ€.
μλ‘μ΄ ν κ΄λ
Έν λ° νμΌμ¦ μ λ₯Ό μ λ³νκΈ° μν΄, MMP-1 νλ‘λͺ¨ν°λ₯Ό μΈκ° κ°μ§μΈν¬μΈ HaCaT μΈν¬μμ μμ μ μΌλ‘ λ°νλλ νμ§μ ν μΈν¬λ₯Ό ꡬμΆνμμΌλ©°, νμμ μ λ³μ ν΅ν΄ MMP-1 νλ‘λͺ¨ν°κ° ν¬ν¨λ pGF1 벑ν°λ‘ HaCaT μΈν¬μ μ±κ³΅μ μΌλ‘ νμ§μ ν λ κ²μ νμΈνμλ€. MMP-1 luciferase λΆμ 쑰건μ ν립νκ³ infection λ μΈν¬μ μμΈμ μ λν λ°μμ λΆμνκΈ° μνμ¬ μμΈμ κ°λμ μκ°μ λ°λ₯Έ luciferase νμ±μ νμΈνμλ€. μ€νκ²°κ³Ό 0.04 J/cm2, 5μκ°μμ κ°μ₯ λμ luciferase νμ±μ λνλ΄μ΄, ν₯ν luciferase assay 쑰건μΌλ‘ κ³ μ νμλ€. μ΄ μΈν¬λ₯Ό μ΄μ©νμ¬, μλ¬Ό μΆμΆλ¬Ό 9κ°λ₯Ό μ λ³νμλ€. κ·Έ κ²°κ³Ό, μ€λ°°μ μΆμΆλ¬Ό(RJE)κ³Ό λ΄μΆ μΆμΆλ―μ΄ UVBμ μνμ¬ μ λλ MMP-1 νλ‘λͺ¨ν° κ²°ν© νμ±μ κ°κ° 80.9%, 75.8%λ‘ μ΅μ νμ¬ κ°μ₯ μ°μν κ΄λ
Έν μ΅μ μμ¬λ‘ μ λ³νμλ€. λν, 25-100 ΞΌg/mLμ λλμμ HaCaT μΈν¬μμ λ
μ±μ΄ λνλμ§ μμλ€.
UVBμ μνμ¬ μ λλ MMP-1 νλ‘λͺ¨ν° κ²°ν© νμ± λ° μΈν¬ λ
μ±μ λν λ€μν RJEμ λλ λ³λ‘ νκ°ν κ²°κ³Ό RJEλ UVBμ μνμ¬ μ λλ MMP-1 νλ‘λͺ¨ν° κ²°ν© νμ±μ λλ μμ‘΄μ μΌλ‘ μ΅μ νλ κ²μΌλ‘ λνλ¬λ€. UVBμ μνμ¬ COX-2μ MMP-1μ λ°νμ΄ μ¦κ°νμμΌλ©°, RJEμ λλ μμ‘΄μ μΌλ‘ COX-2μ MMP-1μ λ°νμ νμ νκ² μ ν΄νμλ€. λν, RJEκ° HaCaT μΈν¬μμ UVBμ μνμ¬ μ λλ MAPKs/MAPKKs/Akt μΈμ°νλ₯Ό λͺ¨λ λλμμ νμ νκ² μ΅μ νμλ€. SKH-1 무λͺ¨ μ₯ λͺ¨λΈμ μ¬μ©ν μ€ν κ²°κ³Όμμ RJEμ 경ꡬ ν¬μ¬κ° UVBμ μνμ¬ μμ±λ μ£Όλ¦μ νμ±κ³Ό λ§μ°μ€ νΌλΆμ‘°μ§μμ COX-2 λ° MMP-13 λ°νμ μ μμ μΌλ‘ μ΅μ νμλ€. μ΄λ¬ν κ²°κ³Όλ RJEκ° COX-2 λ° MMP-1 λ°νμ μ΅μ νλ κ°λ ₯ν νμΌμ¦ λ° κ΄λ
Έν μ΅μ μ λ‘ κ°λ° κ°λ₯μ±μ μ μνκ³ μλ€.
λ λ€λ₯Έ μμ¬λ‘, λ΄μΆ μΆμΆλ¬Ό(CZE)μ΄ HaCaT μΈν¬μμ UVBμ μνμ¬ μ λλ COX-2 λ° MMP-13 λ°νμ μ μνκ² μ΅μ νλ κ²μ νμΈνμλ€. Western blot λΆμ κ²°κ³Όμμ MPAKKs/MAPKsμ μΈμ°νκ° CZEμ μν΄ μ΅μ λμλ€. λν, CZEλ HaCaT μΈν¬μμ UVBμ μνμ¬ μ λλ Akt μΈμ°νμ EGFR λ° Srcμ μΈμ°νλ₯Ό μ μμ μΌλ‘ μ΅μ νμλ€. SKH-1 무λͺ¨ μ₯ λͺ¨λΈμ μ¬μ©ν μ€ν κ²°κ³Όμμλ CZEμ 경ꡬ ν¬μ¬λ UVBμ μνμ¬ μ λλ μ£Όλ¦ νμ±κ³Ό λ§μ°μ€ νΌλΆμ‘°μ§μμ COX-2 λ° MMP-13 λ°νμ μ μνκ² μ΅μ νμλ€. CZEμ μ‘΄μ¬νλ νΉμ νν©λ¬Ό μ€ μ»€νλ―Όμ UVBμ μνμ¬ μ λλ MMP-1 νλ‘λͺ¨ν° κ²°ν© νμ±μ κ°μ₯ λκ² μ΅μ νλ ν¨κ³Όλ₯Ό λνλ΄μλ€.
RJE νν©λ¬Ό μ€ syringic acidμ MMP-1 νλ‘λͺ¨ν° κ²°ν© μ ν΄ νμ±μ΄ κ°μ₯ λκ² λνλ¬λ€. λ°λΌμ syringic acidκ° UVBμ μνμ¬ μ λλ νΌλΆμμ νμ±μ λ―ΈμΉλ μν₯μ λΆμνμλ€. HaCaTμΈν¬μμ syringic acidμΌλ‘ μ²λ¦¬ν λ€, μ μ μμ λ¨λ°±μ§ λ°ν μμ€μ μΈ‘μ νμμΌλ©°, μ΄λ₯Ό ν΅ν΄ syringic acidμ μΈν ROSμ μμ±μ΄ μ‘°μ λ¨μ νμΈνμκ³ , FDAμμ μΉμΈλ νμ°νμ μΈ N-acetyl-L-systein(NAC)μ ν¨κ³Όμ λΉκ΅ν κ²°κ³Ό μ μ¬ν μ ν΄ ν¨κ³Όκ° μμμ λ°νλ€. NADPH μ°ν ν¨μμ syringic acidμ μν₯μ νκ°ν κ²°κ³Ό syringic acidκ° NADPH μ°ν ν¨μμ νμ±μ μ ν΄ν¨μ νμΈνμλ€. Syringic acidμ νΌλΆμ μλ°© κ°λ₯μ±μ νκ°νκΈ° μν΄ λλ¬Όμ€νμ μ€μνμλ€. κ·Έ κ²°κ³Ό, λ§μ±μ μΈ UVB μ²λ¦¬μ μνμ¬ λ¬΄λͺ¨ μ₯μ νΌλΆ μ’
μ λ°μκ³Ό κ·Έμ κ΄λ ¨λ λΆμμ λ°νμ μ΅μ νμλ€. Syringic acidλ NADPH μ°νν¨μμ μ΅μ μ λ‘ μμ©νμ¬ μμΈμ μ μν ROS μμ°μ μ΅μ νκ³ νΌλΆμ λ°μμ λ°©μ§νμ¬, μ²μ° μΉλ£μ λ‘μμ κ°λ₯μ±μ μ μνκ³ μλ€.Excessive ultraviolet (UV) exposure can cause acute skin inflammation and chronic exposure has been linked to skin cancer. While dependent on genetic factors and lifestyle choices, repeated exposure to UV irradiation generally results in the appearance of irregular brown spots and wrinkle formation, collectively referred to as photoaging. The transcription factor AP-1 plays a critical role in these processes via regulation of mmp-1 and cox-2 gene expression, respectively. Due to the fact that AP-1 is a central mediator of UV-induced photoaging and inflammation, the development of analytical tools that efficiently screen compounds that can inhibit AP-1 activity represents a potential strategy to develop new anti-photoaging and anti-inflammatory agents.
To screen effective anti-photoaging and anti-inflammatory agents, I generated immortalized human keratinocyte HaCaT cells stably transfected with an MMP-1 promoter and after selection with puromycin, I confirmed that HaCaT cells were successfully transfected with the pGF1 vector containing the MMP-1 promoter. To determine the optimal conditions needed to assess MMP-1 promoter activity, I investigated different doses of UV and incubation times. The reporter gene assay revealed that 0.04 J/cm2 and 5 h were the optimal conditions for activating the MMP-1 promoter. Using these cells, I screened 99 botanical extracts of interest. 9 botanical extracts showed UVB-induced MMP-1 promoter binding activity inhibition. Rhus javanica extract (RJE) and Curcuma zedoaria extract (CZE) were identified as the most potent anti-photoaging material, suppressing UVB-induced MMP-1 promoter binding activity by 80.9% and 75.8%, respectively. Furthermore, the viability of HaCaT cells did not show signs of cytotoxicity at 25-100 ΞΌg/mL concentrations.
Evaluation of varying RJE concentrations on UVB-induced MMP-1 promoter binding activity and cell cytotoxicity revealed that RJE inhibits UVB-induced MMP-1 promoter binding activity in a dose-dependent manner. I further observed that RJE suppressed UVB-induced MAPKs and AP-1 signaling cascades in HaCaT cells. Experiments using the SKH-1 hairless mouse model revealed that oral administration of RJE significantly suppresses UVB-induced wrinkle formation, as well as COX-2 and MMP-13 expression in mouse skin. These findings suggest that RJE is a potent anti-inflammatory and anti-photoaging agent that inhibits COX-2 and MMP-1 expression.
Several experiments confirmed that CZE significantly suppressed UVB-induced COX-2 and MMP-13 expression in HaCaT cells. My Western blot results showed that phosphorylation of all three MPAKK/MAPKs were suppressed by CZE. Additionally, CZE strongly suppressed UVB-induced Akt phosphorylation as well as EGFR and Src phosphorylation in HaCaT cells. Using an SKH-1 hairless mice model, I determined that CZE prevented chronic UVB-induced wrinkle formation. Immunohistochemistry and Western blot assay results showed that CZE significantly suppressed UVB-induced COX-2 and MMP-13 expression in vivo. Among the specific compounds present in CZE, curcumin was found to exhibit the strongest inhibitory effect on UVB-induced MMP-1 promoter activity.
Among the RJE compounds, syringic acid exhibited the most potent inhibitory effect on MMP-1 promoter activity. I sought to investigate the inhibitory effects of syringic acid on UVB-induced skin carcinogenesis. In vitro experiment, I treated human epidermal keratinocytes (HaCaT cells) with syringic acid and measured the gene and protein expression levels. Accordingly, I detected the change in ROS due to syringic acid treatment, which was compared to the effects of the FDA-approved antioxidant drug N-acetyl-L-cysteine (NAC), which is commonly used to identify and test ROS inducers and to inhibit ROS. Since NADPH oxidases of the Nox family are important enzymatic sources of ROS, I further measured the effect of syringic acid on NADPH oxidase activity to determine the potential targets mediating its inhibitory effects. To evaluate the therapeutic potential of syringic acid, I conducted an in vivo experiment using the SKH-1 hairless mouse model that received topical treatment of syringic acid prior to UVB exposure, and compared the tumor incidence and expression of relevant molecules in the mouse skin.Chapter β
. General Introduction 1
β
-1. Introduction 2
β
-2. Skin carcinogenesis and chemoprevention 4
β
-3. Role of Noxs and its downstream signaling pathways in UV-induced skin carcinogenesis 5
β
-4. Role of EGFR and its downstream signaling pathways in UV-induced skin carcinogenesis 8
β
-5. Role of PTP-ΞΊ as Nox and EGFR signal transmitters in skin cancer 11
β
-6. Preventive botanical extracts and phytochemicals in UV-induced skin damages by NADPH oxidase regulation 13
β
-7. Preventive botanical extracts and phytochemicals in UV-induced skin damages via regulation of EGFR 17
β
-8. References 20
Chapter β
‘. Preventive Effect of Rhus javanica Extract on UVB-induced Skin Inflammation and Photoaging 29
β
‘-1. Introduction 31
β
‘-2. Materials and Methods 34
β
‘-2-1. Materials 34
β
‘-2-2. Sample preparation and extraction procedure 34
β
‘-2-3. Cell culture, UVB exposure and viability assay 35
β
‘-2-4. Animal experiments 35
β
‘-2-5. MMP-1 promoter assay 36
β
‘-2-6. Western blot assay 37
β
‘-2-7. EGFR kinase assay 38
β
‘-2-8. Immunohistochemical analysis 38
β
‘-2-9. Metabolite extraction 39
β
‘-2-10. Chromatograph 39
β
‘-2-11. Statistical analysis 39
β
‘-3. Results 41
β
‘-3-1. RJE inhibits UVB-induced MMP-1 promoter activity in HaCaT cells 41
β
‘-3-2. RJE inhibits UVB-induced phosphorylation of MAPKKs/MAPKs, Akt, EGFR, Src and PKD/PKCΞΌ in HaCaT cells 43
β
‘-3-3. RJE inhibits UVB-induced wrinkle formation and COX-2 and MMP-13 expression in the SKH-1 hairless mouse 48
β
‘-3-4. Identification and quantification of phenolic compounds by LC-MS/MS and effect of RJE compounds on UVB-induced MMP-1 promoter activity 52
β
‘-4. Discussion 57
β
‘-5. Conclusions 60
β
‘-6. References 61
Chapter β
’. Preventive Effect of Curcuma zedoaria Extract on UVBinduced Skin Inflammation and Photoaging 65
β
’-1. Introduction 67
β
’-2. Materials and Methods 70
β
’-2-1. Materials 70
β
’-2-2. Sample preparation and extraction procedure 70
β
’-2-3. Cell culture, UVB exposure, and viability assay 73
β
’-2-4. Animal experiments 73
β
’-2-5. MMP-1 promoter assay 74
β
’-2-6. Western blot assay 75
β
’-2-7. Immunohistochemical analysis 75
β
’-2-8. Metabolite extraction 76
β
’-2-9. Chromatograph 76
β
’-2-10. Statistical analysis 77
β
’-3. Results 78
β
’-3-1. CZE inhibits UVBinduced MMP1 promoter activity, as well as COX2 and MMP13 expression in HaCaT cells 78
β
’-3-2. CZE inhibits UVBinduced phosphorylation of MAPKK/MAPK, Akt, EGFR, and Src in HaCaT cells 81
β
’-3-3. CZE inhibits UVBinduced wrinkle formation and COX2 and MMP13 expression in SKH1 hairless mice 84
β
’-3-4. Identification and quantification of phenolic compounds by LCMS/MS and effect of CZE compounds on UVBinduced MMP1 promoter activity 89
β
’-4. Discussion 94
β
’-5. Conclusions 98
β
’-6. References 99
Chapter β
£. Syringic Acid Prevents Skin Carcinogenesis via Regulation of Nox and EGFR Signaling 104
β
£-1. Introduction 106
β
£-2. Materials and Methods 109
β
£-2-1. Materials 109
β
£-2-2. Cell culture, UVB exposure and viability assay 109
β
£-2-3. Animal experiments 110
β
£-2-4. MMP-1 promoter assay 111
β
£-2-5. PGE2 assay 111
β
£-2-6. Western blot assay 112
β
£-2-7. Measurement of ROS 113
β
£-2-8. PTP-ΞΊ immunoprecipitation 113
β
£-2-9. Histological analysis 114
β
£-2-10. Statistical analysis 114
β
£-3. Results 115
β
£-3-1. Syringic acid inhibits UVB-induced COX-2 and MMP-1 expression, PGE2 production, and MMP-1 promoter activity in HaCaT cells 115
β
£-3-2. Syringic acid inhibits UVB-induced phosphorylation of MAPKs, MAPKKs, and EGFR in HaCaT cells 118
β
£-3-3. Syringic acid inhibits the UVB-induced oxidization of PTP-ΞΊ in HaCaT cells 121
β
£-3-4. Syringic acid and NAC inhibit UVB-induced intracellular ROS generation in HaCaT cells 124
β
£-3-5. Syringic acid prevents UVB-induced skin tumorigenesis in SKH-1 hairless mice 128
β
£-3-6. Syringic acid inhibits UVB-induced COX-2 and MMP-13 expression in SKH-1 hairless mice 131
β
£-4. Discussion 135
β
£-5. Conclusions 139
β
£-6. References 140
κ΅λ¬Έμ΄λ‘ 146λ°
Population Pharmacokinetics and Pharmacogenetics of Tacrolimus in the Early Post-kidney Transplantation Period
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Όλ¬Έ (μμ¬)-- μμΈλνκ΅ λνμ : μ½νκ³Ό, 2013. 2. μ€μ λ―Έ.Tacrolimusλ μ΄μ ν κ±°λΆλ°μ μ΅μ λ₯Ό μνμ¬ μ¬μ©λλ λ©΄μμ΅μ μ μ΄λ€. νμ€ λλκ° νμμ μ₯κΈ° μμ‘΄μ¨κ³Ό μμμ μ§ν λ±μ μ°κ΄ μμ΄ νμ€ λλλ₯Ό λ§μΆλ κ²μ μ€μμ±μ΄ μ΅ν μλ €μ Έ μμΌλ μΉλ£μμ΄ μ’κ³ κ°μΈ κ° λ³μ΄κ° 컀μ μ΄λ₯Ό μ ννκ² μμΈ‘νλ κ²μ μ΄λ €μμ΄ μλ€. Tacrolimusμ μ½λνμ μν₯ μΈμλ‘ μλ €μ Έ μλ κ²λ€λ‘λ λμ΄, μ±λ³, 체μ€, hematocrit, μ΄μ ν κΈ°κ° λ±μ μμ μ§νμ CYP3A5, ABCB1 λ±μ μ μ νμ΄ μλ€. λ³Έ μ°κ΅¬λ μ±μΈ νμμμ μ μ₯ μ΄μ ν μ΄κΈ° 2μ£Όμ νμ€ λλμ λν΄ μ μ νμ κ³ λ €ν μ§λ¨μ½λν μ°κ΅¬λ₯Ό μννμ¬ μ΄μ ν μ΄κΈ° κΈ°κ°μ μ½λνμ μν₯μ μ£Όλ μΈμλ₯Ό κ°λ³νκ³ μ½λ¬Ό λλ μμΈ‘μ μν λͺ¨λΈμ κ°λ°νμ¬, μ΄μ κΈ°λ°ν μ©λ μ μμ νκ³ μ νμλ€.
μ΄μ ν 15μΌκΉμ§ μνν μ΅μ λλμΉλ₯Ό μμ§νκ³ μ΄μ ν¨κ» μ΄μ ν 10-15μΌ μ¬μ΄ tacrolimusμ νμ€ λλ μ‘°λ° μ±νμ μ½λ¬Ό ν¬μ½ ν 0.5, 1, 2, 4, 6, 12 μκ° μ§Έμ μννμ¬ ν¨κ» λΆμνμλ€. λμΌ κΈ°κ°μ λνμ¬ μμμ /μ€νμ€μ κ²μ¬λ₯Ό ν¨κ» μμ§νμκ³ , λͺ¨λ μ°κ΅¬ λμ νμμμ CYP3A5μ ABCB1 μ μ νμ λΆμνμ¬ λͺ¨λΈ ν립μ μ¬μ©νμλ€. λͺ¨λΈ κ°λ°μλ NONMEM version 6μ μ΄μ©νμκ³ , λͺ¨λΈ κ²μ¦μλ visual prediction checkμ bootstrap 2000νλ₯Ό μννμλ€.
μ°κ΅¬μλ μ 체 122λͺ
μ νμκ° ν¬ν¨λμκ³ , μ΄ μ€ 61λͺ
μμ μ‘°λ° μ±νμ μννμλ€. λ°μ΄ν° λΆμ κ²°κ³Ό first-order absorption and eliminationμ μ΄μ©ν one-compartment modelλ‘, lag timeμ μ μ© κ²½μ°μ κ°μ₯ μ μ€λͺ
λμλ€. λͺ¨λΈμ μ§λ¨ ν΄λ¦¬μ΄λ°μ€(CL/F)λ 20.6 L/hλ‘ μΆμ° λμκ³ , λΆν¬ μ©μ (Vd/F)μ 286 L, ν‘μ μμ(Ka)λ 4.41 h-1λ‘ κ³μ° λμμΌλ©° lag timeμ 0.25 hr λ‘ κ³ μ νμλ€. μ΄μ ν κΈ°κ°μ΄ μ¦κ°ν¨μ λ°λΌ tacrolimus ν΄λ¦¬μ΄λ°μ€λ μ¦κ°νμκ³ CYP3A5 μ μ ν *3/*3μ 보μ ν νμλ *1μ 보μ ν νμκ΅°λ³΄λ€ tacrolimus ν΄λ¦¬μ΄λ°μ€κ° 36.7% κ°μνμλ€. (p < 0.001) λν λΆν¬ μ©μ μ 체μ€μ λΉλ‘νμ¬ μ¦κ°νλ κ²μΌλ‘ λνλ¬λ€.
λ³Έ μ°κ΅¬λ μ μ₯ μ΄μμ λ°μ νκ΅μΈ νμμμ μ΄μ ν μ΄κΈ°μμ μ‘°λ° μ±νκ³Ό μ΅μ λλμΉ κ²°κ³Όλ₯Ό ν¨κ» μ΄μ©νμ¬ tacrolimusμ κ°μΈκ° μ½λν μ°¨μ΄μ μν₯μ λ―ΈμΉλ μμΈμ κ°λ³νμλ€. λ³Έ μ°κ΅¬μμ κ°λ°λ λͺ¨λΈμ ν΅ν΄ λ³΄λ€ μ ν©νκ² tacrolimusμ μ©λμ μμΈ‘ν μ μμ κ²μ΄λ©°, μ΄λ κ°μΈλ§μΆ€ μ½λ¬Όμλ²μ κΈ°λ°μ΄ λ κ²μ΄λ€.μ μ½ i
λͺ© μ°¨ iii
List of Tables iv
List of Figures v
μ λ‘ 1
μ°κ΅¬ λ°©λ² 4
μ°κ΅¬ κ²°κ³Ό 13
κ³ μ°° 17
μ°Έκ³ λ¬Έν 22
Tables & Figures 27
Abstract 40Maste
λ² μ΄λΉλΆμΈλμ μν΄ν μ£Όκ±°μμ μ μν μ μ± λ°©μ μ°κ΅¬(Housing policy directions for the retired bany-room generation in Korea)
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ΈνΈ : μ΄ μ°κ΅¬λ³΄κ³ μμ λ΄μ©μ κ΅ν μ°κ΅¬μμ μ체 μ°κ΅¬λ¬Όλ‘μ μ λΆμ μ μ±
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