• Title/Summary/Keyword: C-Reactive Protein

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Role of Ischemic Preconditioning in the Cardioprotective Mechanisms of Monomeric C-Reactive Protein-Deposited Myocardium in a Rat Model

  • Kim, Eun Na;Choi, Jae-Sung;Kim, Chong Jai;Kim, So Ra;Oh, Se Jin
    • Journal of Chest Surgery
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    • v.54 no.1
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    • pp.9-16
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    • 2021
  • Background: The deposition of monomeric C-reactive protein (mCRP) in the myocardium aggravates ischemia-reperfusion injury (IRI) and myocardial infarction. Ischemic preconditioning (IPC) is known to protect the myocardium against IRI. Methods: We evaluated the effects of IPC on myocardium upon which mCRP had been deposited due to IRI in a rat model. Myocardial IRI was induced via ligation of the coronary artery. Direct IPC was applied prior to IRI using multiple short direct occlusions of the coronary artery. CRP was infused intravenously after IRI. The study included sham (n=3), IRI-only (n=5), IRI+CRP (n=9), and IPC+IRI+CRP (n=6) groups. The infarcted area and the area at risk were assessed using Evans blue and 2,3,5-triphenyltetrazolium staining. Additionally, mCRP immunostaining and interleukin-6 (IL-6) mRNA reverse transcription-polymerase chain reaction were performed. Results: In the IRI+CRP group, the infarcted area and the area of mCRP deposition were greater, and the level of IL-6 mRNA expression was higher, than in the IRI-only group. However, in the IPC+IRI+CRP group relative to the IRI+CRP group, the relative areas of infarction (20% vs. 34%, respectively; p=0.079) and mCRP myocardial deposition (21% vs. 44%, respectively; p=0.026) were lower and IL-6 mRNA expression was higher (fold change: 407 vs. 326, respectively; p=0.376), although the difference in IL-6 mRNA expression was not statistically significant. Conclusion: IPC was associated with significantly decreased deposition of mCRP and with increased expression of IL-6 in myocardium damaged by IRI. The net cardioprotective effect of decreased mCRP deposition and increased IL-6 levels should be clarified in a further study.

Associations of intermediate hyperglycemia with elevated abdominal obesity, high-sensitivity C-reactive protein, and leptin in Korean adults

  • Heashoon Lee
    • Journal of Korean Biological Nursing Science
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    • v.26 no.3
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    • pp.250-258
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    • 2024
  • Purpose: This study investigated the associations between intermediate hyperglycemia (IH) and increased body mass index (BMI), abdominal obesity (AO), high-sensitivity C-reactive protein (hs-CRP), and leptin levels in Korean adults. Methods: The participants were 248 adults (≥ 19 years) who understood the purpose of the study, had no cognitive impairment, and were able to communicate. Physical examinations, BMI, AO measurements, and blood tests were performed. Data were analyzed using the t-test, chi-square test, Pearson correlation coefficients, and multiple logistic regression analyses. The risk factors for IH were predicted after adjusting for BMI, waist circumference (WC), age, hs-CRP and leptin levels, education, and economic status. Results: WC, hs-CRP and leptin levels, and age were higher in the IH group than in the non-IH group. According to the multiple logistic regression analysis, the factors affecting IH prevalence were WC, hs-CRP, leptin, and age. AO (male, WC ≥ 90 cm; female, WC ≥ 85 cm) exhibited an adjusted odds ratio of 5.45 for IH. IH was 2.43 times higher in those with hs-CRP > 3 mg than in those with hs-CRP < 1 mg. As leptin levels increased, the odds ratio for IH increased by 3.05 times. IH was 8.07, 8.79, 18.42, and 35.33 times more common for those in their 30s, 40s, 50s, and ≥ 60 years of age, respectively, than those 19-29 years old. Conclusion: This study provides evidence that interventions for AO should be included in IH management programs. Identifying the predictive factors for IH may contribute to the early detection of type 2 diabetes mellitus.

Differences in Body Weight, Dietary Efficiency, Brain Obesity Control Factor (AMPK), Reactive Oxygen Species (MDA), and Antioxidant Enzymes (SOD) in Young Mice According to the Intensity of Aerobic Exercise for 8 Weeks (8주간의 유산소 운동강도에 따른 어린 생쥐의 체중, 식이효율, 뇌의 비만조절 인자(AMPK), 활성산소(MDA), 항산화효소(SOD)의 차이)

  • Jeon, Mi Yang
    • Journal of Korean Biological Nursing Science
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    • v.23 no.3
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    • pp.247-255
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    • 2021
  • Purpose: The goal of this study was to see how different aerobic exercise intensities affected AMP-activated protein kinase (AMPK), reactive oxygen, and antioxidant enzymes in young mice during an 8-week period. Methods: Forty male C57BL/6 mice, aged seven weeks, were randomly assigned to one of four groups: control (n=10), low-intensity exercise (n=10), moderate-intensity exercise (n=10), and high-intensity exercise (n=10). For eight weeks, aerobic activity was performed once a day for 35-40 minutes, five days a week. The data were analyzed using descriptive statistics, analysis of variance (ANOVA), chi-squared tests, and the Tukey test in the SPSS/WIN 25.0 program. Results: Weight (p=.001) was substantially different between the moderate-intensity exercise group and the control group in AMPK (p<.001). In addition, there were no significant differences between the moderate-intensity exercise group and the control group in reactive oxygen malondialdehyde (MDA) levels (p=.136) and antioxidant enzyme superoxide dismutase (SOD) levels (p=.521). Conclusion: These findings suggest that moderate-intensity aerobic exercise increased AMPK activation and helped young mice shed weight.

Role of biomarkers in antimicrobial stewardship: physicians' perspectives

  • Hyeri Seok;Dae Won Park
    • The Korean journal of internal medicine
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    • v.39 no.3
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    • pp.413-429
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    • 2024
  • Biomarkers are playing an increasingly important role in antimicrobial stewardship. Their applications have included use in algorithms that evaluate suspected bacterial infections or provide guidance on when to start or stop antibiotic therapy, or when therapy should be repeated over a short period (6-12 h). Diseases in which biomarkers are used as complementary tools to determine the initiation of antibiotics include sepsis, lower respiratory tract infection (LRTI), COVID-19, acute heart failure, infectious endocarditis, acute coronary syndrome, and acute pancreatitis. In addition, cut-off values of biomarkers have been used to inform the decision to discontinue antibiotics for diseases such as sepsis, LRTI, and febrile neutropenia. The biomarkers used in antimicrobial stewardship include procalcitonin (PCT), C-reactive protein (CRP), presepsin, and interleukin (IL)-1β/IL-8. The cut-off values vary depending on the disease and study, with a range of 0.25-1.0 ng/mL for PCT and 8-50 mg/L for CRP. Biomarkers can complement clinical diagnosis, but further studies of microbiological biomarkers are needed to ensure appropriate antibiotic selection.

Metformin Induces Lipogenesis and Apoptosis in H4IIE Hepatocellular Carcinoma Cells

  • Deokbae Park;Sookyoung Lee;Hyejin Boo
    • Development and Reproduction
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    • v.27 no.2
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    • pp.77-89
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    • 2023
  • Metformin is the most widely used anti-diabetic drug that helps maintain normal blood glucose levels primarily by suppressing hepatic gluconeogenesis in type II diabetic patients. We previously found that metformin induces apoptotic death in H4IIE rat hepatocellular carcinoma cells. Despite its anti-diabetic roles, the effect of metformin on hepatic de novo lipogenesis (DNL) remains unclear. We investigated the effect of metformin on hepatic DNL and apoptotic cell death in H4IIE cells. Metformin treatment stimulated glucose consumption, lactate production, intracellular fat accumulation, and the expressions of lipogenic proteins. It also stimulated apoptosis but reduced autophagic responses. These metformin-induced changes were clearly reversed by compound C, an inhibitor of AMP-activated protein kinase (AMPK). Interestingly, metformin massively increased the production of reactive oxygen species (ROS), which was completely blocked by compound C. Metformin also stimulated the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK). Finally, inhibition of p38MAPK mimicked the effects of compound C, and suppressed the metformin-induced fat accumulation and apoptosis. Taken together, metformin stimulates dysregulated glucose metabolism, intracellular fat accumulation, and apoptosis. Our findings suggest that metformin induces excessive glucose-induced DNL, oxidative stress by ROS generation, activation of AMPK and p38MAPK, suppression of autophagy, and ultimately apoptosis.

Cedrela sinensis Leaves Suppress Oxidative Stress and Expressions of iNOS and COX-2 via MAPK Signaling Pathways in RAW 264.7 Cells

  • Bak, Min-Ji;Jeong, Jae-Han;Kang, Hye-Sook;Jin, Kyong-Suk;Ok, Seon;Jeong, Woo-Sik
    • Preventive Nutrition and Food Science
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    • v.14 no.4
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    • pp.269-276
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    • 2009
  • Overproduction of reactive oxygen species (ROS), including nitric oxide (NO), could be associated with the pathogenesis of various diseases such as cancer and chronic inflammation. Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are known to play key roles in the development of these diseases. Cedrela sinensis leaves have been used in Asian countries as a traditional remedy for enteritis, dysentery and itching. In the present study, we investigated the anti-inflammatory effects of Cedrela sinensis leaves in lipopolysaccharide (LPS)- stimulated RAW 264.7 macrophages. Powder of C. sinensis leaves was extracted with 95% ethanol and fractionated with a series of organic solvents including n-hexane, dichloromethane, ethyl acetate, n-butanol, and water. The dichloromethane (DCM) fraction strongly inhibited NO production possibly by down-regulating iNOS and COX-2 expression, as determined by Western blotting. Hydrogen peroxide-induced generation of reactive oxygen species (ROS) was also effectively inhibited by the DCM fraction from C. sinensis leaves. In addition, C. sinensis inhibited LPS-mediated p65 activation via the prevention of IκB-$\alpha$ phosphorylation. Furthermore, mitogen-activated protein kinases (MAPKs) such as ERK 1/2 and p38 were found to affect the expression of iNOS and COX-2 in the cells. Taken together, our data suggest that leaves of C. sinensis could be used as a potential source for anti-inflammatory agents.

Comparative Study of Autophagy in Oxaliplatin-Sensitive and Resistant SNU-C5 Colon Cancer Cells

  • Boo, Sun-Jin;Piao, Mei Jing;Kang, Kyoung Ah;Zhen, Ao Xuan;Fernando, Pincha Devage Sameera Madushan;Herath, Herath Mudiyanselage Udari Lakmini;Lee, Seung Joo;Song, Seung Eun;Hyun, Jin Won
    • Biomolecules & Therapeutics
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    • v.30 no.5
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    • pp.447-454
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    • 2022
  • Few studies have evaluated the role of autophagy in the development of oxaliplatin (OXT) resistance in colon cancer cells. In this study, we compared the role of autophagy between SNU-C5 colon cancer cells and OXT-resistant SNU-C5 (SNU-C5/OXTR) cells. At the same concentration of OXT, the cytotoxicity of OXT or apoptosis was significantly reduced in SNU-C5/OXTR cells compared with that in SNU-C5 cells. Compared with SNU-C5 cells, SNU-C5/OXTR cells exhibited low levels of autophagy. The expression level of important autophagy proteins, such as autophagy-related protein 5 (Atg5), beclin-1, Atg7, microtubule-associated proteins 1A/1B light chain 3B I (LC3-I), and LC3-II, was significantly lower in SNU-C5/OXTR cells than that in SNU-C5 cells. The expression level of the autophagy-essential protein p62 was also lower in SNU-C5/OXTR cells than in SNU-C5 cells. In SNU-C5/OXTR cells, the production of intracellular reactive oxygen species (ROS) was significantly higher than that in SNU-C5 cells, and treatment with the ROS scavenger N-acetylcysteine restored the reduced autophagy levels. Furthermore, the expression of antioxidant-related nuclear factor erythroid 2-related factor 2 transcription factor, heme oxygenase-1, and Cu/Zn superoxide dismutase were also significantly increased in SNU-C5/OXTR cells. These findings suggest that autophagy is significantly reduced in SNU-C5/OXTR cells compared with SNU-C5 cells, which may be related to the production of ROS in OXT-resistant cells.

Baicalin Improves the IL-6-Mediated Hepatic Insulin Resistance in Hepa-1c1c7 Cells

  • Chae, Byeong Suk;Oh, Chanho
    • Natural Product Sciences
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    • v.19 no.4
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    • pp.360-365
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    • 2013
  • Baicalin has antioxidant, anti-inflammatory and anti-diabetic properties. IL-6 is a primary proinflammatory cytokine that contributes to impaired insulin signaling in liver. This study was carried out to investigate whether baicalin improves IL-6-mediated insulin resistance in liver. Hepa-1c1c7 cells were pre-treated with 50 and 100 ${\mu}M$ baicalin in complete media for 1 h and then cultured in the presence or absence of IL-6 (20 ng/ml). These results demonstrated that baicalin restored IL-6-suppressed expression of insulin receptor substrate (IRS)-1 protein, downregulated IL-6-increased gene expression of C-reactive protein (CRP) and suppressor of cytokine signaling (SOCS)-3, and inhibited LPS-induced production of IL-6 in Hepa-1c1c7 cells. These findings indicate that baicalin may ameliorate hepatic insulin resistance via improvement of IL-6-mediated impaired insulin signaling in hepatocytes.

Rabbit Antibody Raised against Murine Cyclin D3 Protein Overexpressed in Bacterial System

  • Jun, Do-Youn;Kim, Mi-Kyung;Kim, Young-Ho
    • Journal of Microbiology and Biotechnology
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    • v.6 no.6
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    • pp.474-481
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    • 1996
  • Since the commercially available rabbit anti-cyclin D3, generated from c-terminal 16 amino acid residues which are common to human and murine cyclin D3, is highly cross-reactive with many other cellular proteins of mouse, a new rabbit polyclonal anti-cyclin D3 has been raised by using murine cyclin D3 protein expressed at a high level in Escherichia coli as the immunogen. To express murine cyclin D3 protein in E. coli, the cyclin D3 cDNA fragment encoding c-terminal 236 amino acid residues obtained by polymerase chain reaction (PCR) was inserted into the NcoI/BamHI site of protein expression vector, pET 3d. Molecular mass of the cyclin D3 overexpressed in the presence of IPTG (Isopropyl $\beta$-D-thiogalactopyranoside) was approximately 26 kDa as calculated from the reading frame on the DNA sequence, and the protein was insoluble and mainly localized in the inclusion bodies that could be easily purified from the other cellular soluble proteins. When renaturation was performed following denaturation of the insoluble cyclin D3 protein in the inclusion bodies using guanidine hydrochloride, 4.4 mg of soluble form of cyclin D3 protein was produced from the transformant cultured in 100ml of LB media under the optimum conditions. Four-hundred micrograms of the soluble form of cyclin D3 protein was used for each immunization of a rabbit. When the antiserum obtained 2 weeks after tertiary immunization was applied to Western blot analysis, it was able to detect 33 kDa cyclin D3 protein in both murine lymphoma cell line BW5147.G.1.4 and human Jurkat T cells at 3,000-fold dilution with higher specificity to murine cyclin D3, demonstrating that the new rabbit polyclonal anti-murine cyclin D3 generated against c-terminal 236 amino acid residues more specifically recognizes murine cyclin D3 protein than does the commercially available rabbit polyclonal antibody raised against c-terminal 16 amino acids residues.

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