The aim of the study was to assess the effect of a polyunsaturated omega-3 fatty acids (PUFA) supplementation on the parameters of body composition, muscle strength and physical performance in elderly people with decreased muscle mass (DMM). Fifty three elderly people with an ALM index (the ratio of appendicular lean mass to squared height) either below (−2SD: low muscle mass-LMM) or between (−1SD and −2SD: the risk of LMM-rLMM) the ALM index for the young Polish reference population were randomly assigned to PUFA-treated groups (LMM-PUFA, rLMM-PUFA) or control groups (LMM-control, rLMM-control). PUFA-treated groups received capsules containing 1.3 g of PUFA and 10 mg of vitamin E, while the control groups received 11 mg of vitamin E daily for 12 weeks. Body composition (BIA analysis), muscle strength (hand grip measured with dynamometer) and physical performance (Timed Up and Go test-TUG) were assessed before and after supplementation. No statistically significant differences were observed either in muscle mass or in the hand grip and TUG in any group. The post-pre difference (mean ± SD) in ALM index was as follows (kg/m²): LMM-PUFA: 0.00 ± 0.30, rLMM-PUFA: 0.00 ± 0.22, LMM-control: 0.03 ± 0.36, rLMM-control: –0.03 ± 0.20. In our study, a 12 week supplementation of PUFA did not affect the evaluated parameters in elderly individuals with DMM.

Though historically regarded as an inert energy store, adipose tissue is a complex endocrine organ, which is increasingly implicated in the pathogenesis of inflammatory bowel disease (IBD). Accumulating evidence points to visceral adipose tissue and specifically to its mesenteric component, or “creeping fat” as impacting on the disease course through its immunomodulatory properties. On the one hand, mesenteric fat acts as a physical barrier to inflammation and is involved in controlling host immune response to translocation of gut bacteria. On the other hand, however, there exists a strong link between visceral fat and complicated course of the disease with unfavorable therapeutic outcomes. Furthermore, “creeping fat” appears to play different roles in different IBD phenotypes, with the greatest pathogenetic contribution probably to an ileal form of Crohn’s disease. In this review, we summarize and discuss the existing literature on the subject and identify high-priority areas for future research. It may be that a better understanding of the role of mesenteric fat in IBD will determine new therapeutic targets and translate into improved clinical outcomes.

Intercellular adhesion molecule‐1 (ICAM‐1) has been implicated in adhesion of colorectal and pancreatic cancer cells (of the SW480 and PSN‐1 line, respectively) to the peritoneal mesothelium. It has been demonstrated that ICAM‐1 expression increases with senescence in some cell types, however, the significance of this phenomenon in the context of malignant dissemination remains elusive. In this report we show that the adherence of SW480 and PSN‐1 cells to senescent human omentum‐derived mesothelial cells (HOMCs) in vitro is greater than to early‐passage cells and that the effect is mediated by ICAM‐1. Senescent HOMCs display increased expression of ICAM‐1 mRNA and cell surface protein. The development of this phenotype is related to increased oxidative stress in senescent cells. The augmented ICAM‐1 expression in HOMCs can be reduced by culturing cells with antioxidants; in contrast, exposure of HOMCs to an oxidant, t‐BHP, leads to cellular senescence and increased ICAM‐1 expression. The effect is partly mediated by activation of p38 MAPK and AP‐1 signaling pathways. Finally, culture of HOMCs in the presence of a strong antioxidant, PBN, significantly reduces the senescence‐associated increase in SW480 and PSN‐1 cancer cell binding. These results indicate that increased oxidative stress and increased expression of ICAM‐1 in senescent HOMCs may facilitate peritoneal adhesion of selected colorectal and pancreatic cancers.

The objective of this study was to evaluate the usefulness of a hydroalcoholic extract from Galinsoga parviflora herb (GP) in some aspects of the endothelial cell function necessary for anti-inflammatory activity and wound healing and relate these to the GP phytochemical profile. This study demonstrated that the GP extract caused a dose-dependent reduction of IL-6 secretion on IL-1β-stimulated endothelial cells. The IL-6 release was decreased to 33% ± 9% while this did not influence the IL-6 secretion without stimulation. Additionally, the GP extract exhibited an anti-hyaluronidase activity (IC₅₀ = 0.47 mg/mL), which was evidently stronger than the positive control kaempferol (IC₅₀ = 0.78 mg/mL) as well as a moderate and concentration-dependent, antioxidant activity. The results of the scratch assay showed that exposure of the endothelial cells to GP induced complete healing of the damage after 12 h of the study. The phytochemical profile of the extract was studied by using spectrophotometric (total amount of polyphenols and flavonoids) and UPLC (phenolic acids) methods. The main compound in the GP extract was a chlorogenic acid (2.00 ± 0.01 mg/g by UPLC). The total content of polyphenols was 98.30 ± 0.14 mg of chlorogenic acid equivalent/g of the dry herb and content of flavonoids amounted to 6.15 ± 0.41 mg quercetin equivalent/g of the dry herb. Moreover, the presence of flavonoids in G. parviflora was provided after their isolation and identification by spectroscopic methods. In conclusion, it demonstrated that application of GP in the treatment of skin lesions gives possibility of wound healing based on antioxidant, anti-inflammatory, and hyaluronidase-inhibiting activities of G. parviflora herb extract.

Thrombin, the ligand of the protease-activated receptor 1 (PAR1), is a well-known stimulator of proangiogenic responses in vascular endothelial cells (ECs), which are mediated through the induction of vascular endothelial growth factor (VEGF). However, the transcriptional events underlying this thrombin-induced VEGF induction and angiogenic response are less well understood at present. As reported here, we conducted detailed promotor activation and signal transduction pathway studies in human microvascular ECs, to decipher the transcription factors and the intracellular signaling events underlying the thrombin and PAR-1-induced endothelial VEGF induction. We found that c-FOS is a key transcription factor controlling thrombin-induced EC VEGF synthesis and angiogenesis. Upon the binding and internalization of its G-protein-coupled PAR-1 receptor, thrombin triggers ERK1/2 signaling and activation of the nuclear AP-1/c-FOS transcription factor complex, which then leads to VEGF transcription, extracellular secretion, and concomitant proangiogenic responses of ECs. In conclusion, exposure of human microvascular ECs to thrombin triggers signaling through the PAR-1–ERK1/2–AP-1/c-FOS axis to control VEGF gene transcription and VEGF-induced angiogenesis. These observations offer a greater understanding of endothelial responses to thromboinflammation, which may help to interpret the results of clinical trials tackling the conditions associated with endothelial injury and thrombosis.