Effects of Albumin Infusion on Serum Levels of Albumin, Proinflammatory Cytokines (TNF-α, IL-1, and IL-6), CRP, and MMP-8; Tissue Expression of EGRF, ERK1, ERK2, TGF-β, Collagen, and MMP-8; and Wound Healing in Sprague Dawley RatsRead the full article
International Journal of Inflammation publishes papers on the molecular basis, cell biology and pharmacology of inflammation, including acute/chronic inflammation and the cellular processes/molecular mechanisms involved in inflammatory responses.
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Evaluation of Inflammatory Markers in Patients Undergoing a Short-Term Aerobic Exercise Program while Hospitalized due to Acute Exacerbation of COPD
Introduction. Acute exacerbation is an important factor for a worse prognosis in patients with chronic obstructive pulmonary disease (COPD). It promotes the increase of the inflammatory process and worsens quality of life, lung function, and muscle weakness. It is believed that physical exercise performed during the exacerbation breaks the vicious cycle of systemic manifestations without an increase in the inflammatory process. Objective. To evaluate the influence of short-term aerobic physical exercise during hospitalization on inflammatory markers. Patients and Methods. 26 patients were evaluated (69.2% female, FEV 137.5 ± 12.9%, and age 68.4 ± 11.6 years) 24 hours after hospitalization for smoking history, Charlson index, quality of life, systemic inflammatory markers, and body composition. After 48 hours of hospitalization, all patients underwent a 6-minute walk test (6MWT) and a new spirometry test, and BODE index was calculated. After 72 hours of hospitalization, patients in the intervention group underwent aerobic exercise on a treadmill for 15 minutes twice daily; before and after the aerobic exercise, blood samples were collected for evaluation of inflammatory markers. Finally, a month after hospital discharge, all patients were reevaluated according to systemic inflammatory markers, quality of life, body composition, spirometry, 6MWT, and BODE index. Results. Patients of both groups did not differ in severity of disease and general characteristics. The intervention group did not show worsening in the inflammatory process after aerobic activity: TNF-α from 1.19 (0 99–1.71) to 1.21 (0.77–1.53) (), IL-6 from 2.41 (2.02–0.58) to 2.66 (1.69–0.48) (), and CRP from 3.88 (2.26–8.04) to 4.07 (2.65–13.3) (). There was a negative correlation between the IL-6 marker and the 6MWT; that is, with the reduction in inflammatory levels, there was an improvement in exercise capacity one month after hospital discharge. Conclusion. The present study showed that the aerobic physical activity initiated during hospitalization in patients with exacerbated COPD did not worsen the inflammatory process.
JNK Signaling Pathway Suppresses LPS-Mediated Apoptosis of HK-2 Cells by Upregulating NGAL
Objective. To explore the role of the c-Jun N-terminal kinase (JNK) signaling pathway in upregulated NGAL expression and its antiapoptotic mechanism in lipopolysaccharide (LPS)-mediated renal tubular epithelial cell injury. Methods. In vitro, HK-2 cells were divided into five groups (Con, LPS 1 h, LPS 3 h, LPS 6 h, and LPS 12 h groups) based on the time of LPS (10 μM) treatment. NGAL and caspase-3 gene expression levels were detected by RT-PCR to assess dynamic changes. HK-2 cells were pretreated with SP600125 (20 μM) for 2 hours, followed by LPS (10 μM) stimulation for 3 hours. NGAL and caspase-3 gene expression levels were then determined. Results. NGAL mRNA was increased significantly within 6 hours, and caspase-3 mRNA was increased within 3 hours after treatment (). Correlation analysis showed a high correlation between their expression (r = 0.448, ). After pretreatment with SP600125, mRNA expression of NGAL in the LPS group was inhibited, while that of caspase-3 was increased significantly. The NGAL mRNA expression level in the SB + LPS group was decreased significantly compared with that in the LPS group, but it was slightly higher than that in the SP group (∼1.5 times of that in the Con group). However, caspase-3 mRNA expression was increased significantly in the SB + LPS group () (3.5 times of that in the Con group). It also showed a significant increase compared with SP and LPS groups ( vs. SB group; vs. LPS group). We also found that NGAL and caspase 3 proteins were increased significantly in LPS and SP + LPS groups, but SP600125 decreased the NGAL level by almost 35% and increased the caspase 3 level by 50% in the SP + LPS group compared with the LPS group (). Conclusions. The JNK signaling pathway inhibits LPS-mediated apoptosis of renal tubular epithelial cells by upregulating NGAL.
Inhibition of Proinflammatory Cytokines in Cutibacterium acnes-Induced Inflammation in HaCaT Cells by Using Buddleja davidii Aqueous Extract
Acne is an inflammatory skin disorder; although some anti-inflammatory medicines for treating acne are available in a market, they have considerable side effects; therefore, new treatment options are needed. In the present study, among the 16 aqueous extracts of plants collected from Jeju Island in Korea which are used to test anti-inflammatory activity, B. davidii showed the strong decline of the proinflammatory cytokine expression against the inflammatory process caused by C. acnes in Human HaCaT keratinocyte cells. B. davidii downregulated the expression of 57% of COX-2, 41% of iNOS, and proinflammatory cytokines 29% of TNF-α, 32% of IL-1β, 21% of IL-6, and 35% of IL-8. Furthermore, B. davidii inhibited NF-κB and MAPK signaling cascades in keratinocytes that activated by toll-like receptor 2 (TLR-2) in response to C. acnes. Given those results, B. davidii is a potential agent to reduce the proinflammatory cytokine expression against C. acnes-induced inflammation and might provide an alternative to the current medications.
Therapeutic Effects of the Combination of Alpha-Lipoic Acid (ALA) and Coenzyme Q10 (CoQ10) on Cisplatin-Induced Nephrotoxicity
Background. Nephrotoxicity of cisplatin has been recognized since its introduction more than 25 years ago. However, despite intense efforts to develop less toxic and equally effective alternatives, cisplatin continues to be widely prescribed. Aim and Objectives. The study is aimed at assessing the possible prophylactic effect of coenzyme Q10 (CoQ10) and alpha-lipoic acid (ALA) (separately or in combination) on experimentally cisplatin-induced nephrotoxicity. Subjects and Methods. An experimental study was performed on adult male albino rats (n = 40), weighing 200–250 g. Rats were randomly divided into 5 groups: group I (normal saline control), group II (cisplatin control), group III (CoQ10 and cisplatin), group IV (ALA and cisplatin), and group V (CoQ10, ALA, and cisplatin). CoQ10 and/or ALA were given as pretreatment for 9 days, followed by cisplatin injection in the 10th day of the study, followed by a short posttreatment course for 3 days. Renal functions, tissue antioxidant activity, and inflammatory markers (tumor necrosis factor, TNF) were estimated along with histopathological study. Results. Renal function tests and urinary proteins were significantly higher within group II compared with other groups ( value <0.001). Creatinine clearance was significantly higher with combination therapy (group V compared to other groups). Both TNF and malondialdehyde (MDA) were significantly higher within group II whereas GSH content, catalase, and superoxide dismutase (SOD) were significantly lower in group II. MDA level was significantly lower when combination therapy was used. Marked renal damage was histologically detected in the cisplatin group, whereas the least renal damage was noticed in the combination group. Conclusion. The study confirmed the role of antioxidants in preventing nephrotoxicity caused by cisplatin; the prophylactic effect of combined therapy with CoQ10 and ALA is superior to that of monotherapy.
Methylation Pattern of the SOCS3 and IL6R Promoters in Rheumatoid Arthritis
Interleukin-6 (IL-6) plays an essential function in the development of rheumatoid arthritis (RA), mainly through its proinflammatory effect, which may lead to joint destruction. The genes encoding IL-6 receptor (IL6R) and suppressor of cytokine signaling 3 (SOCS3) play a key role in the IL-6 signaling pathway, but their epigenetic regulation remains unclear. The aim of the study was to investigate how the presence of methylation in the SOCS3 and IL6R promoters is associated with the morbidity and severity of RA. A total of 146 unrelated individuals, 122 with RA and 24 healthy controls, were enrolled in the study. All subjects were genotyped with regard to the rs4969168 and rs4969170 polymorphisms in the SOCS3 gene and the rs2228145 and rs4129267 polymorphisms in IL6R. The methylation study included 52 patients with RA and 24 healthy controls. Qualitative real-time methylation-specific PCR was used to evaluate methylation status. We found no differences between patients and healthy controls in the methylation pattern in the IL6R and SOCS3 promoter regions and in variants frequency. The methylation profiles of the SOCS3 and IL6R promoters do not support the hypothesis that the genes SOCS3 and IL6R involved in the JAK-STAT signaling pathway are epigenetically deregulated in whole blood.
Caveolin-1 Scaffolding Domain Peptide Regulates Colon Endothelial Cell Survival through JNK Pathway
It has been reported that pathological angiogenesis contributes to both experimental colitis and inflammatory bowel disease. Recently, we demonstrated that endothelial caveolin-1 plays a key role in the pathological angiogenesis of dextran sodium sulfate (DSS) colitis. However, the molecular mechanism of caveolin-1 regulation of endothelial function is unknown. In this study, we examined how the antennapedia- (AP-) conjugated caveolin-1 scaffolding domain (AP-Cav) modulates vascular endothelial growth factor- (VEGF-) dependent colon endothelial cell angiogenic responses, as seen during colitis. We used mouse colon endothelial cells and found that AP-Cav significantly inhibited VEGF-mediated bromodeoxyuridine (BrdU) incorporation into colon microvascular endothelial cells. AP-Cav significantly blunted VEGF-dependent extracellular signal-regulated kinase 1/2 (ERK 1/2) phosphorylation at 10 minutes and 2 hours after stimulation, compared with the AP control peptide. AP-Cav + VEGF-A treatment also significantly increased c-Jun N-terminal kinase (JNK) phosphorylation at 2 hours. AP-Cav + VEGF-A treatment significantly downregulated retinoblastoma (Rb) protein levels, upregulated cleaved caspase-3 protein levels at 4 hours, and induced apoptosis. Thus, our study suggests that disruption of endothelial caveolin-1 function via the AP-Cav diverts VEGF signaling responses away from endothelial cell proliferation and toward apoptosis through the inhibition of mitogen-activated protein (MAP) kinase signaling and the induction of JNK-associated apoptosis.