• 생명과학회지
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• 제34권6호
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• pp.408-417
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• 2024

원화(Daphne genkwa (Siebold & Zucc))의 50% 에탄올 추출물인 PB-81이 소 로타바이러스 설사병 환축에서 설사병의 치료효과와 바이러스 증식 억제 효과가 나타나는가를 확인하였다. PB-81에 의해 상피세포주인 A549 세포와 혈액세포주인 NK92 세포에서 각각 IFN-β와 IFN-γ가 유도되는 것을 확인하였다. PB-81의 바이러스의 증식억제 효과를 확인하기 위해 PB-81을 MBDK 세포에 바이러스의 감염 전, 동시, 감염 후에 투여하는 세 가지 경우에서 바이러스 억제효과를 확인한 결과 PB-81을 투여한 모든 경우에서 바이러스가 억제되었으며, 바이러스 감염 전에서 투여하는 경우에서 가장 좋은 바이러스 억제효과가 나타났다. 마우스에서의 독성검사에서는 투여최대용량인 20 mg/mL에서도 독성에 따른 부작용이 나타나지 않았다. 소 로타바이러스 설사병 환축 16두와 대조군 4두를 대상으로 한 치료효과 검증에는 20 mg/5 mL 용량의 PB-81을 투여한 결과, PB-81을 투여한 모든 소 로타바이러스 설사병 환축이 완치되었으며 PB-81의 투여 후에 완치까지 소요된 기간은 PB-81투여군이 평균 2.25일이었고, PB-81을 투여하지 않은 대조군이 6.5일로 PB-81의 투여에 의한 소 로타바이러스 설사병의 치료효과가 나타나는 것을 확인하였으며 PB-81을 투여한 모든 환축에서 부작용이 검출되지 않았다.

• Biomolecules & Therapeutics
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• 제32권4호
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• pp.481-491
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• 2024

Paxlovid is the first approved oral treatment for coronavirus disease 2019 and includes nirmatrelvir, a protease inhibitor targeting the main protease (M^pro) of SARS-CoV-2, as one of the key components. While some specific mutations emerged in M^pro were revealed to significantly reduce viral susceptibility to nirmatrelvir in vitro, there is no report regarding resistance to nirmatrelvir in patients and animal models for SARS-CoV-2 infection yet. We recently developed xenograft tumors derived from Calu-3 cells in immunodeficient mice and demonstrated extended replication of SARS-CoV-2 in the tumors. In this study, we investigated the effect of nirmatrelvir administration on SARS-CoV-2 replication. Treatment with nirmatrelvir after virus infection significantly reduced the replication of the parental SARS-CoV-2 and SARS-CoV-2 Omicron at 5 days post-infection (dpi). However, the virus titers were completely recovered at the time points of 15 and 30 dpi. The virus genomes in the tumors at 30 dpi were analyzed to investigate whether nirmatrelvir-resistant mutant viruses had emerged during the extended replication of SARS-CoV-2. Various mutations in several genes including ORF1ab, ORF3a, ORF7a, ORF7b, ORF8, and N occurred in the SARS-CoV-2 genome; however, no mutations were induced in the M^pro sequence by a single round of nirmatrelvir treatment, and none were observed even after two rounds of treatment. The parental SARS-CoV-2 and its sublineage isolates showed similar IC₅₀ values of nirmatrelvir in Vero E6 cells. Therefore, it is probable that inducing viral resistance to nirmatrelvir in vivo is challenging differently from in vitro passage.

• 대한약침학회지
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• 제27권1호
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• pp.1-13
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• 2024

Background: Diabetic nephropathy (DN) is one of the major complications of chronic hyperglycaemia affecting normal kidney functioning. The ayurvedic medicine curcumin (CUR) is pharmaceutically accepted for its vast biological effects. Objectives: The Curcuma-derived diferuloylmethane compound CUR, loaded on Poly (lactide-co-glycolic) acid (PLGA) nanoparticles was utilized to combat DN-induced renal apoptosis by selectively targeting and modulating Bcl2. Methods: Upon in silico molecular docking and screening study CUR was selected as the core phytocompound for nanoparticle formulation. PLGA-nano-encapsulated-curcumin (NCUR) were synthesized following standard solvent displacement method. The NCUR were characterized for shape, size and other physico-chemical properties by Atomic Force Microscopy (AFM), Dynamic Light Scattering (DLS) and Fourier-Transform Infrared (FTIR) Spectroscopy studies. For in vivo validation of nephro-protective effects, Mus musculus were pre-treated with CUR at a dose of 50 mg/kg b.w. and NCUR at a dose of 25 mg/kg b.w. (dose 1), 12.5 mg/kg b.w (dose 2) followed by alloxan administration (100 mg/kg b.w) and serum glucose levels, histopathology and immunofluorescence study were conducted. Results: The in silico study revealed a strong affinity of CUR towards Bcl2 (dock score -10.94 Kcal/mol). The synthesized NCUR were of even shape, devoid of cracks and holes with mean size of ~80 nm having -7.53 mV zeta potential. Dose 1 efficiently improved serum glucose levels, tissue-specific expression of Bcl2 and reduced glomerular space and glomerular sclerosis in comparison to hyperglycaemic group. Conclusion: This study essentially validates the potential of NCUR to inhibit DN by reducing blood glucose level and mitigating glomerular apoptosis by selectively promoting Bcl2 protein expression in kidney tissue.

• IMMUNE NETWORK
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• 제24권3호
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• pp.15.1-15.18
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• 2024

Osteoarthritis (OA) involves cartilage degeneration, thereby causing inflammation and pain. Cardiovascular diseases, such as dyslipidemia, are risk factors for OA; however, the mechanism is unclear. We investigated the effect of dyslipidemia on the development of OA. Treatment of cartilage cells with low-density lipoprotein (LDL) enhanced abnormal autophagy but suppressed normal autophagy and reduced the activity of transcription factor EB (TFEB), which is important for the function of lysosomes. Treatment of LDL-exposed chondrocytes with rapamycin, which activates TFEB, restored normal autophagy. Also, LDL enhanced the inflammatory death of chondrocytes, an effect reversed by rapamycin. In an animal model of hyperlipidemia-associated OA, dyslipidemia accelerated the development of OA, an effect reversed by treatment with a statin, an anti-dyslipidemia drug, or rapamycin, which activates TFEB. Dyslipidemia reduced the autophagic flux and induced necroptosis in the cartilage tissue of patients with OA. The levels of triglycerides, LDL, and total cholesterol were increased in patients with OA compared to those without OA. The C-reactive protein level of patients with dyslipidemia was higher than that of those without dyslipidemia after total knee replacement arthroplasty. In conclusion, oxidized LDL, an important risk factor of dyslipidemia, inhibited the activity of TFEB and reduced the autophagic flux, thereby inducing necroptosis in chondrocytes.

• 대한한의학방제학회지
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• 제15권1호
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• pp.185-197
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• 2007

Objective : This study was conducted to investigate the effects of Hwangryunhaedok-Tang and Geongangbuja-Tang on the change of interleukin-6 (IL-6) and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) level induced by LPS I.C.V. injection in mice. Method : We devided group into 6 mice and 6 mice were assingned to each group. In the normal group only saline was administered intragastrically, and in the control group LPS was injected intracerebroventricularly 1 hr after intragastric administration of saline. In the experiment groups Hwangryunhaedok-Tang(0.5g/kg, 1.0g/kg, 3.0g/kg) was administered intragastrically to mice 1 hr prior to LPS(100mg/mouse) I.C.V. injection.. Also Geongangbuja-Tang (0.5g/kg, 1.0g/kg, 3.0g/kg) was administered intragastrically to mice 1 hr prior to LPS(100mg/mouse) I.C.V. injection. To measure the plasma IL-6 and $TNF-{\alpha}$ level of mice, their blood samples were collected from retro-orbital plexus, immediately centrifuged at $4^{\circ}C$, and plasma was removed and stored frozen at $-83^{\circ}C$ for later determination of IL-6 and $TNF-{\alpha}$. The level of IL-6 and $TNF-{\alpha}$ production was measured by enzyme-linked immunosorbent assay in the plasma. Result : Regarding IL-6 level, The 0.5g/kg and the 1g/kg groups of Geongangbuja-Tang decreased IL-6 level. Especially the 3g/kg control group decreased IL-6 level significantly than the normal group(p<0.01). Regarding $TNF-{\alpha}$ level, the 3g/kg group of Geongangbuja-Tang decreased it significantly(p<0.05). Conclusion : These data revealed that Hwangryunhaedok-Tang might not have the anti imflammatory effect and Geongangbuja-Tang(3g/kg)might have the anti imflammatory effect by reducing the plasma IL-6 and $TNF-{\alpha}$ level in mice LPS Injection.EIM (Eighteen Incompatible Medicaments) is an important component in Oriental pharmacology and is directly related to clinical prescriptions. Medical practitioners argued that the definite cause and meaning of EIM was ambiguous and therefore debated the issue of clinical application of the EIM. This study conducted an in-depth literary research on the origin, meaning and contents of EIM with the purpose to contribute in its efforts to be used clinically. Even after thousands of years have past since establishment of Oriental medicine, EIM is still tabooed and was an obstacle that hindered ideologies. Modern herbal medicine texts claim that the use of EIM can reduce treatment effects and promote poisoning and side effects. However, since long ago, there has been medical practitioners who reject this as false. Recently, poisoning caused by EIM has been claimed to be from the toxicity of the drug itself, rather than the result of interaction between the drugs, and therefore they suggest that EIM is not a forbidden domain. In addition, EIM showed a difference in number depending on the era. However, this can be understood not as a definite number, but instead as a warning to be careful during combination of drugs for use as clinical medicine. Historically, there were very few cases in which EIM was used for clinical tests and thus, the clinical value is not, while others applied EIM directly to their bodies, which showed signs for the usefulness and potential of EIM for us. A more concrete and in-depth study must be made on EIM.

• Tuberculosis and Respiratory Diseases
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• 제57권4호
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• pp.351-357
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• 2004

연구배경 : 최근 항암화학요법과 방사선요법의 병용치료는 국소진행성 비소세포폐암 치료에 있어서 표준치료방법으로 자리잡고 있으며 동시요법이 순차적요법에 비해 치료반응율에 있어서 우수하다고 알려져 있다. 본 연구는 비소세포폐암 치료에 있어서 우수한 효과를 보이고 방사선감작 효과가 있다고 알려진 paclitaxel (60 $mg/m^2$) 매주투여와 동시 방사선요법의 III병기 비소세포폐암 환자에서의 치료효과와 독성을 조사하기 위하여 시행하였다. 방 법 : III병기 비소세포폐암 환자 22명 (IIIA:6, IIIB:16)을 대상으로 paclitaxel (60 $mg/m^2$)을 제 1, 8, 15, 22, 29, and 36일째에 매주 투여하고 동시에 54 Gy의 방사선 치료를 시행하였다. 초기 동시치료를 종료하고 paclitaxel (175 $mg/m^2$)/cisplatin (75 $mg/m^2$) 혹은 paclitaxel (175 $mg/m^2$)/carboplatin (6AUC) regimen 으로 보강화학요법을 3주 간격으로 2주기 시행하였다. 결 과 : 전반적 치료반응율은 81.8% (18/22)로서 완전관해가 9.1% (2/22), 부분관해가 72.7% (16/22)의 결과를 보였다. 두명의 (9.1%) 환자가 치료종료 후 방사선폐장염의 합병증으로 사망하였다. 3도 이상의 독성 반응은 방사선폐장염 (22.7%), 식도염 (22.7%), 신경병증 (13.6%), 및 백혈구감소증 (13.6%)의 결과를 나타내었다. 중앙생존기간은 15개월이었고 1년 및 2년 생존율은 각각 63.6%와 31.8%였다. 결 론 : 국소진행성 비소세포폐암 환자에서 paclitaxel 매주 투여에 의한 동시 방사선요법은 우수한 종양반응율을 나타내지만 치명적인 방사선폐장염의 발생 위험이 있으므로 향후 보완연구가 필요할 것으로 사료된다.

• 대한수의학회지
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• 제41권4호
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• pp.571-578
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• 2001

방사선 피폭선량의 예측을 위한 방사선 민감 지표 모델 개발의 일환으로 apoptotic fragment assay법이 방사선에 피폭된 후 체내 피폭선량을 예측할 수 있는 지표로의 이용 가능성을 평가하기 위하여 코발트-60 감마선과 의료용 싸이크로트론 50MeV($p{\rightarrow}Be^+$) fast neutron 을 0.25Gy에서 1Gy의 선량을 마우스에 각각 전신 조사한 후 소장 음와세포내 apoptotic crypt cell의 수적 변화를 관찰하였다. 저선량 조사군에서 apoptotic crypt cell의 출현 빈도가 1Gy까지 급격하게 증가한 것으로 보아 방사선이 stem cell 지역에 있는 crypt cell의 형태학적 변화를 유발하는 것으로 나타났다. 이상의 결과는 아포토시스가 손상된 세포를 제거하므로 손상된 방사선 민감 표적 장기의 항상성 유지에 중요한 역할을 하는 것으로 판단되었다. Apoptotic fragments의 발생빈도에 대한 선량-반응 곡선에 있어서 음와세포는 중성자조사군이 $y=0.18+(9.728{\pm}0.887)D+(-4.727{\pm}1.033)D^2$ ($r^2=0.984$)으로, 반면에 감마선조사군은 $y=0.18+(5.125{\pm}0.601)D+(-2.652{\pm}0.7000)D^2$ ($r^2=0.970$)의 식을 얻었다. 이와 같이 중성자조사군과 감마선조사군은 공히 linear quadratic model 로 관찰되었다. apoptotic fragments 의 발생빈도와 조사 선량간에 유의한 효과가 있는 것으로 확인되었다. 이상의 결과에서 조사선량의 증가에 비례하여 방사선 민감 세포의apoptotic fragments 가 수적으로 증가하였으며, 고준위 방사선과 저준위 방사선은 선량 반응 관계식과 시간 경과에 따른 영향이 매우 유사하였으며, 마우스 음와세포의 apoptosis 유도에 대한 중성자선의 방사선 생물학적 효과비(RBE)는 2.072이였다. 그리고 모든 방사선조사군에서 방사선피폭 후 4시간과 6시간에 apoptosis 유도가 가장 많았으며, 음와세포의 형태학적 소견은 정상 대조군에서 관찰되지 않는 전형적인 apoptotic fragments 가 나타났다. 따라서 음와 세포에서의 아포토시스 유도는 방사선 피폭으로 발생된 세포 손상의 생물학적 영향 평가검색, 방사선 방호제의 민감도 검사, 방사성 동위원소의 체내 오염에 대한 체내 피폭선량 예측의 지표 및 방사선 민감 표적장기의 손상정도 파악에 이용 가능할 것임. Apoptotic fragment assay 법은 0.25Gy에서 1Gy 까지의 선량에서 간편하고 빠르며 재현성이 있는 지표로서 방사선 민감 표적 장기의 선량 반응 평가와 방사선 피폭후 조기 피폭선량 예측을 위한 방사선 생물학적 선량측정법의 좋은 지표로 사용할 수 있을 것으로 사료됨.

• 대한미생물학회지
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• 제21권3호
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• pp.311-329
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• 1986

The experimental exposure of animals to sources of ultraviolet radiation (UVR) which emit their energy primarily in the UVB region (280-320nm) is known to result in a number of well-described changes in the recipient's immune competence. Two such changes include a depressed capacity to effectively respond immunologically to transplants of syngeneic UVR tumors and a markedly reduced responsiveness to known inducers of delayedtype (DTH) and contact hypersensitivity (CH) reactions. The results of experiments that were designed to elucidate the mechanisms responsible for UVR-induced immunomodulation have implicated: 1) an altered pattern of lymphocyte recirculation, 2) suppressor T cells(Ts), 3) deviations in systemic antigen presenting cell (APC) potential. 4) changes in the production of interleukin-1-like molecules, and 5) the functional inactivation of epidermal Langerhans cells in this process. The exposure of skin to UVR, therefore, causes a number of both local and systemic alterations to the normal host immune system. In spite of this seeming complexity and diversity of responses, our recent studies have established that each of the UVR-mediated changes is probably of equal importance to creating the UVR-induced immunocompromised state. Normal animals were exposed to low dose UVR radiation on their dorsal surfaces under conditions where a $3.0\;cm^2$ area of skin was physically protected from the light energy. Contact sensitization of these animals with DNFB, to either the irradiated or protected back skin, resulted in markedly reduced CH responses. This was observed in spite of a normal responsiveness following the skin sensitization to ventral surfaces of the UVR-exposed animals. Systemic treatment of the low dose UVR recipients with the drug indomethacin (1-3 micrograms/day) during the UVR exposures resulted in a complete reversal of the depressions observed following DNFB sensitization to "protected" dorsal skin while the altered responsiveness found in the group exposed to the skin reactive chemical through directly UVR-exposed sites was maintained. These studies implicate the importance of EC as effective APC in the skin and also suggest that some of the systemic influences caused by UVR exposure involve the production of prostaglandins. This concept was further supported by finding that indomethacin treatment was also capable of totally reversing the systemic depressions in CH responsiveness caused by high dose UVR exposure (30K joules/$m^2$) of mice. Attempts to analyze the cellular mechanisms responsible established that the spleens of all animals which demonstrated altered CH responses, regardless of whether sensitization was through a normal or an irradiated skin site, contained suppressor cells. Interestingly, we also found normal levels of T effector cells in the peripheral lymph nodes of the UVR-exposed mice that were contact sensitized through normal skin. No effector cells were found when skin sensitization took place through irradiated skin sites. In spite of such an apparent paradox, insight into the probable mechanisms responsible for these observations was provided by establishing that UVR exposure of skin results in a striking and dose-dependent blockade of the efferent lymphatic vessels in all peripheral lymph nodes. Therefore, the afferent phases of immune responses can apparently take place normally in UVR exposed animals when antigen is applied to normal skin. The final effector responses, however, appear to be inhibited in the UVR-exposed animals by an apparent block of effector cell mobility. This contrasts with findings in the normal animals. Following contact sensitization, normal animals were also found to simultaneously contain both antigen specific suppressor T cells and lymph node effector cells. However, these normal animals were fully capable of mobilizing their effector cells into the systemic circulation, thereby allowing a localization of these cells to peripheral sites of antigen challenge. Our results suggest that UVR is probably not a significant inducer of suppressor T-cell activity to topically applied antigens. Rather, UVR exposure appears to modify the normal relationship which exists between effector and regulatory immune responses in vivo. It does so by either causing a direct reduction in the skin's APC function, a situation which results in an absence of effector cell generation to antigens applied to UVR-exposed skin sites, inhibiting the capacity of effector cells to gain access to skin sites of antigen challenge or by sequestering the lymphocytes with effector cell potential into the draining peripheral lymph nodes. Each of these situations result in a similar effect on the UVR-exposed host, that being a reduced capacity to elicit a CH response. We hypothesize that altered DTH responses, altered alloresponses, and altered graft-versus-host responses, all of which have been observed in UVR exposed animals, may result from similar mechanisms.

• 대한약리학회지
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• 제7권1호
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• pp.53-65
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• 1971

It is well known that diabetes mellitus is associated with metabolic derangements, such as hyper-glycemia, ketosis, glycosuria, and also widespread alterations in the blood vessels, kidneys, eyes, peripheral nerves and heart. It is also recognized that healing of skin wound is delayed in diabetics. In bone, according to Aegerter, osteopenia develops in diabetes mellitus and it is chiefly ascribed to overutilization of protein. Shim claims that total blood flow to the entire skeletal system is approximately 4 to 8 percent of resting cardiac output and blood supply to the skeletal system would be decreased on account of secondary arteriosclerotic changes in the diabetics. An adequate blood supply is an essential factor in the healing process of fracture, and disturbed blood flow, either local or systemic, will invariably delay union of the fragments or the fragments from being fused. As the author has encountered several cases of diabetics in whom healing of fracture was delayed or incomplete, this experimental study was undertaken to elucidate the effects of hyperglycemia and diabetes mellitus on the healing process of fracture. In this experiment adult albino rabbits, weighing about 2 kg. were used and divided into 6 groups. The femur of each animal was fractured surgically, and then the healing process of fracture was periodically checked by radiography at an interval of one week for a period of 6 weeks. Thereafter, all the rabbits were killed to obtain tissue preparation of the femur. The experimental groups were as follows; 1) Control group: Six rabbits sustained a surgical fracture to the femur, without being given any other treatment or drug. 2) Alloxan-treated group: For inducing diabetes, alloxan was given intravenously to 17 rabbits in various dose as follows; to 7 of them 40 mg/kg, to 6 rabbits 80 mg/kg and to 4 rabbits 120 mg/kg of body weight, respectively. 3) Insulin-treated group: Protamine-zinc insulin was injected subcutaneously to each of 6 rabbits in a daily dose of 1 unit per kilogram of body weight. 4) Group treated with insulin after alloxan: Four rabbits were given 80 mg of alloxan once and than 1 unit of insulin per kilogram of body weight daily. Another 5 rabbits were injected 1 unit of insulin per kg of body weight daily following administration of alloxan in a dose of 120 mg/kg. 5) Homotransplantation group: Following intravenous injection of alloxan in a dose of 120 mg/kg, 10 rabbits underwent homotransplantation of a short bone segment to the femur. Five of them were subsequently given 1 unit/kg of insulin daily. 6) Sugar-treated group: six rabbits were fed $15{\sim}20$ gm of sugar daily throughout the period of experiment. The results obtained are summarized as follows; 1. Blood sugar level and damage to the pancreatic islet increased proportionately when alloxan was given to the rabbits in various doses. No appreciable change could be observed in the islets when the blood sugar level was altered by either oral administration of sugar or subcutaneous injection of insulin. 2. Comparing with the control group, healing of fracture was delayed in the alloxan-treated group, while callus formation and periosteal reaction were shown to be more prominent in this group and subsequently, the ultimate osseous tissue formed at the fracture site was significantly smaller in amount and less compact. These findings were more marked as the amount of alloxan increased. 3. Administration of insulin prevented the delay in healing process of fracture in the rabbits with alloxan-induced hyperglycemia. In this case, the course and progression of fracture healing were almost similar to those of control group. 4. Union between the host bone and the fragment transplanted from other rabbit of the same species was more delayed in the group treated with alloxan alone than in the group to which insulin was administered after development of alloxan-induced diabetes. In both groups periosteal new bone developed from the ends of the host bone, above and below the transplanted fragment, and directly fused with failure of periosteal callus to bridge the adjacent ends of the host bone and the transplanted fragment. 5. The healing process of fracture was not inhibited by alteration in blood sugar level when the blood sugar was abnormally increased by excessive sugar intake or lowered by administration of insulin alone. The healing of fracture in these groups progressed similarly as in the control group. In brief summary, it appears that the healing process of fracture would be definitely disturbed in diabetic state brought about by damage to the pancreatic islet. As such an inhibition could be overcome with insulin, it seems that insulin plays an important role in healing of fracture, but alteration in blood sugar level alone does not modify healing process of fracture to significant degree.

• 한국식품영양과학회지
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• 제33권1호
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• pp.52-58
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• 2004

배추김치의 생리활성물질인 3-(4-hydroxyl-3',5'-dimethoxyphenyl)propionic acid의 고지혈증 치료효과를 살펴보기 위하여 고콜레스테롤 혈증을 유발시킨 토끼에게 1차 실험에서는 정상식이를 공급하고 2차 실험에서는 고콜레스테롤 식이를 공급하면서 각각 16일간 정맥으로 투여하여 혈장지질 농도 변화를 살펴보았고, 그 효과는 고지혈증 치료제로 사용되고 있는 Simvastatin과 비교하였다. 정상식이 공급시 Kimchi군 및 Simvastatin군에 의한 총콜레스테롤 감소는 대조군에 비해 18.65%와 29.67%이었고 고콜레스테롤 식이 공급시에는 각각 33.79%및 21.81%이었다. LDL-C의 저하현상은 정상식이 공급시에는 미미하게 관찰되었고, 고콜레스테롤 식이 공급시에는 Kimchi군 및 Simvastatin군에서 약 130%정도의 감소 효과가 관찰되었다. 중성지방의 감소효과는 정상식이시에는 거의 관찰되지 않았고, 고콜레스테롤 식이시에는 Kimchi군에서 약 105%, 그리고 Simvastatin군에서 약 62%정도의 감소가 관찰되었다. HDL-C의 변화는 모든 군에서 관찰되지 않았다. 고콜레스테롤 식이를 섭취한 토끼간의 HMG-CoA reductase 활성을 살펴보았을 때 Kimchi군 및 Simvastatin군의 활성이 48.44% 그리고 139.06% 증가하였다. 본 연구결과 Kimchi군은 고지혈증을 치료하는 효과가 있음이 관찰되었고, 그 효과는 Simvastatin군과 유사하였다. Kimchi군 및 Simvastatin군에서 관찰된 HMG-CoA reductase 활성의 증가는 지질저하 현상에 대한 보상 작용으로 생체 항상성 유지를 위한 현상으로 사료된다 3-(4-hydroxyl-3',5'-dimethoxyphenyl)propionic acid의 고지혈증 치료기전은 Simvastatin과 유사할 것으로 예상된다.