• 대한임상검사과학회지
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• 제49권2호
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• pp.121-127
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• 2017

이 연구에서는 복부비만을 가진 고령여성을 대상으로 대사증후군 동반 유무에 따른 대사증후군 위험요인과 hs-CRP와의 관련성에 대해 알아보고자 하였다. 대사증후군 진단은 AHA/NHLBI (American Heart Association/National Heart, Lung and Blood Institute) 2005년 기준에 따라 5가지 기준 중 3개 이상 해당되는 경우 대사증후군 진단군(MetS, N=77), 2개이하의 위험요인에 해당하는 경우 대조군(Absent, N=97)으로 분류하였다. hs-CRP 농도는 대사증후군 위험요인과 밀접한 관련이 있으며, 특히 복부비만(r=0.190, p=0.014), 공복혈당(r=0.240, p=0.002), HDL-콜레스테롤(r=-0.164, p=0.035)과 연관이 있음을 확인할 수 있었다. 또한 대조군보다 대사증후군 진단군에서 hs-CRP가 높게 나타났으며(p=0.007), 복부비만 상태일지라도 높은 혈당(p=0.006)과 낮은 HDL-콜레스테롤혈증(p=0.010)의 위험요인이 있는군에서 hs-CRP가 높았다. 결론적으로 복부비만이 있더라도 대사증후군 위험요인의 동반 유무에 따라 염증관련 위험도가 달라짐을 알 수 있었다.

• 생명과학회지
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• 제17권10호
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• pp.1419-1425
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• 2007

비만 여자 중학생을 대상으로 12주간 12주간 유산소운동과 저항운동을 병행한 복합운동 프로그램을 실시한 결과는 다음과 같다. 본 연구에서 체중감소와 체지방의 감소에 따른 CRP와 아디포넥틴 농도의 개선을 기대하였지만 유의한 변화가 없었다. 본 연구에서는 다음과 같은 결론을 내린다. 1. 12주간의 중강도 운동 프로그램은 혈장 CRP와 혈장 아디포넥틴의 유용한 개선에 영향을 미치지 않는다. 2. 운동에 의한 인슐린저항성은 이러한 특별한 혈장 염증 지표들의 농도 변화에 의해 설명되어지지 않는다. 이상으로 본 연구에서 처방된 운동프로그램은 신체조성과 인슐린저항성의 변화에는 긍정적인 영향을 미쳤지만 이러한 인자의 개선에도 불구하고 CRP와 아디포넥틴 농도의 변화에는 영향을 미치지 못하였다. 따라서 앞으로 16주 이상의 운동기간과 운동강도에 따른 복합운동 프로그램의 실시가 CRP와 아디포넥틴의 변화에 미치는 영향과 CRP의 발현에 관련인자인 $TNF-{\alpha}$, IL-6 등과 같은 인자들의 변화에 미치는 추가적인 연구가 필요하다.

• 보건행정학회지
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• 제31권2호
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• pp.158-172
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• 2021

Background: Metabolic syndrome has been known as a risk of cardiovascular disease. Meanwhile, high sensitivity C-reactive protein (hs-CRP) is used as a predictor of cardiovascular disease. In this paper, we aimed to investigate the association between hs-CRP and metabolic syndrome. Method: A total of 7,633 were chosen as the study population from the 7th Korea National Health and Nutrition Examination Survey dataset (2016-2017). Our dependent variable was whether an individual had metabolic syndrome or not, and the independent variable of interest was hs-CRP which was categorized into three groups. The chi-square tests and hierarchical logistic regression analyses reflecting survey characteristics were conducted. All analyses were stratified by gender. Results: According to the adjusted model with all covariates, compared to individuals having the low risk of hs-CRP, those having its average risk were more likely to have metabolic syndrome in men (odds ratio [OR], 1.41; 95% confidence interval [CI], 1.12-1.76) and women (OR, 1.69; 95% CI, 1.33-2.16). Individuals having the high risk was not significantly different in men; however, they were more likely to have metabolic syndrome in women (OR, 2.03; 95% CI, 1.28-3.23). Conclusion: In an upcoming aging society, it is important to reduce the risk of metabolic syndrome to improve population health. This study suggests that hs-CRP may be used as a marker of the risk of metabolic syndrome in a gender-specific way, thereby contributing to enhancing awareness of the risk of metabolic syndrome among the general public.

• The Korean Journal of Pain
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• 제23권2호
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• pp.147-150
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• 2010

Background: Chronic low back pain can be a manifestation of lumbar degenerative disease, herniation of intervertebral discs, arthritis, or lumbar stenosis. When nerve roots are compromised, low back pain, with or without lower extremity involvement, may occur. Local inflammatory processes play an important role in patients with acute lumbosciatic pain. The purpose of this study was to assess the value of erythrocyte sedimentation rate (ESR) and high sensitivity C-reactive protein (hsCRP) measurements in patients with chronic low back pain or radiculopathy. Methods: ESR and hsCRP were measured in 273 blood samples from male and female subjects with low back pain and/or radiculopathy due to herniated lumbar disc, spinal stenosis, facet syndrome, and other diseases. The hsCRP and ESR were measured prior to lumbar epidural steroid injection. Results: The mean ESR was 18.8 mm/h and mean hsCRP was 1.1 mg/L. ESR had a correlation with age. Conclusions: A significant systemic inflammatory reaction did not appear to arise in patients with chronic low back pain.

• Journal of Veterinary Science
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• 제21권6호
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• pp.89.1-89.6
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• 2020

Two miniature Schnauzer dogs with chronic pancreatitis were investigated. Both dogs showed systemic hypertension and increased concentrations of triglycerides and C-reactive protein. Abdominal radiography revealed cylindrical calcification in the retroperitoneum, and computed tomography (CT) showed extensive calcification of the abdominal and peripheral arteries in both dogs. Metastases and other dystrophic conditions that can cause arterial calcification were excluded based on the laboratory tests, and the dogs were diagnosed with atherosclerosis ante mortem. Atherosclerosis should be considered when extensive arterial calcification is observed on abdominal radiography or CT in miniature Schnauzers.

• 한국콘텐츠학회논문지
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• 제19권11호
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• pp.375-382
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• 2019

임신 초기 염증으로 인한 영양막세포의 기능 이상은 C-reactive protein (CRP)의 발현을 증가시켜 산모와 태아의 상호작용에 영향을 미침으로써, 조산 및 자간전증 등을 유발한다. 그러나, CRP 발현 조절과 관련된 생체표지자 발굴 및 개발은 미흡한 실정이다. 본 연구는 염증이 유발된 영양막세포에서 증가된 CRP 발현과 관련된 miRNA를 발굴 및 그 발현을 분석함으로써, miRNA를 통해 영양막세포 염증 조절 기전에 관여하는 생체표지자를 밝히고자 한다. miRNA 데이터베이스(mirna, TargetScan, MicroCosm)에서 공통적으로 CRP 유전자 발현을 조절할 것으로 예측되는 miR-7, miR-150, miR-186, 그리고 miR-424를 선별하여 HTR-8/SVneo에 LPS (20ng/mL)를 처리하여 in vitro 상에서 염증 반응을 유도하였다. 각각의 miRNAs의 발현을 qRT-PCR 방법으로 비교 분석하였다. 그 결과, LPS 처리된 영양막세포에서 CRP의 발현은 유의성 있게 증가되었다(p<0.001). miR-150와 miR-424는 발현이 유의성 있게 감소됨을 확인하였다(p<0.001). 따라서, 염증이 유도된 영양막세포에서의 CRP 발현을 조절하는 기전에 miR-150와 miR-424가 관여하는 것을 의미하며, 향후 염증성 산과질환의 산전 진단에 유용한 자료로 사용될 것으로 사료된다.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2007년도 제48회 학술심포지움 및 추계국제학술대회
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• pp.64.1-64.1
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• 2007

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• 한국임상수의학회지
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• 제38권2호
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• pp.103-103
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• 2021

• BMB Reports
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• 제56권12호
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• pp.663-668
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• 2023

C-reactive protein (CRP) is an inflammatory marker and risk factor for atherosclerosis and cardiovascular diseases. However, the mechanism through which CRP induces myocardial damage remains unclear. This study aimed to determine how CRP damages cardiomyocytes via the change of mitochondrial dynamics and whether survivin, an anti-apoptotic protein, exerts a cardioprotective effect in this process. We treated H9c2 cardiomyocytes with CRP and found increased intracellular ROS production and shortened mitochondrial length. CRP treatment phosphorylated ERK1/2 and promoted increased expression, phosphorylation, and translocation of DRP1, a mitochondrial fission-related protein, from the cytoplasm to the mitochondria. The expression of mitophagy proteins PINK1 and PARK2 was also increased by CRP. YAP, a transcriptional regulator of PINK1 and PARK2, was also increased by CRP. Knockdown of YAP prevented CRP-induced increases in DRP1, PINK1, and PARK2. Furthermore, CRP-induced changes in the expression of DRP1 and increases in YAP, PINK1, and PARK2 were inhibited by ERK1/2 inhibition, suggesting that ERK1/2 signaling is involved in CRP-induced mitochondrial fission. We treated H9c2 cardiomyocytes with a recombinant TAT-survivin protein before CRP treatment, which reduced CRP-induced ROS accumulation and reduced mitochondrial fission. CRP-induced activation of ERK1/2 and increases in the expression and activity of YAP and its downstream mitochondrial proteins were inhibited by TAT-survivin. This study shows that mitochondrial fission occurs during CRP-induced cardiomyocyte damage and that the ERK1/2-YAP axis is involved in this process, and identifies that survivin alters these mechanisms to prevent CRP-induced mitochondrial damage.

• BMB Reports
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• 제46권2호
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• pp.119-123
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• 2013

Methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), an endogenous neurotoxin, is known to perform a role in the pathogenesis of Parkinson's disease (PD). In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with salsolinol. When cytochrome c was incubated with salsolinol, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in salsolinol-treated cytochrome c. Salsolinol also led to the release of iron from cytochrome c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the salsolinol-mediated cytochrome c modification and carbonyl compound formation. It is suggested that oxidative damage of cytochrome c by salsolinol might induce the increase of iron content in cells, subsequently leading to the deleterious condition which was observed. This mechanism may, in part, provide an explanation for the deterioration of organs under neurodegenerative disorders such as PD.