The term inflammaging is now widely used to designate the inflammatory process of natural aging. During this process, cytokine balance is altered, presumably due to the loss of homeostasis, thus contributing to a greater predisposition to disease and exacerbation of chronic diseases. The aim of the study was to analyze the relationship between pro-inflammatory markers and age in the natural aging process of healthy individuals. One hundred and ten subjects were divided into 5 groups according to age (22 subjects/group). Interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were quantified using the ELISA method. High-sensitivity C-reactive protein (hsCRP) was analyzed by turbidimetry according to laboratory procedures. The main findings of this study were: a positive correlation between hsCRP and IL-6 as a function of age (110 subjects); women showed stronger correlations; the 51-60 age group had the highest values for hsCRP and IL-6; women presented higher values for hsCRP in the 51-60 age group and higher values for IL-6 in the 61-70 age group; and men showed higher values in the 51-60 age group for hsCRP and IL-6. In conclusion, the natural aging process increased IL-6 and hsCRP levels, which is consistent with the inflammaging theory; however, women presented stronger correlations compared to men (IL-6 and hsCRP) and the 51-60 age range seems to be a key point for these increases. These findings are important because they indicate that early preventive measures may minimize the increase in these inflammatory markers in natural human aging.

The pulp of jussara açaí (Euterpe edulisMartius) fruit is rich in anthocyanins that exert antioxidant and anti-inflammatory effects similar to those exerted by aerobic exercise. In the present study, we investigated the effects of jussara açaí fruit pulp consumption, either alone or in combination with aerobic exercise, on the hepatic oxidative and inflammatory status of ApoE-deficient (ApoE^− / −) mice. Male mice were divided into four groups (control (C), control plus açaí, exercise plus açaí (EXA) and exercise (EX)) and fed the AIN-93M diet or the AIN-93M diet formulated to contain 2 % freeze-dried açaí pulp. Mice in the EX and EXA groups were subjected to a progressive running programme (5 d/week, 60 min/d, 16 m/min) for 12 weeks. Mice that were made to exercise exhibited reduced (40·85 %;P< 0·05) hepatic superoxide dismutase activity when compared with the C mice, independent of the açaí diet. Mice in the EX group exhibited a lower (42 %;P< 0·05) mRNA expression of monocyte chemotactic protein-1 in the liver compared with the C mice. Mice in the EXA and EX groups had lower percentages of hepatic lipid droplets (70 % and 56 %, respectively;P< 0·05) when compared with the C mice. Mice in the EX group had smaller (58 %;P< 0·05) area of lesions in the aorta when compared with the C mice. Serum lipid profile was not affected (P>0·05). In conclusion, aerobic exercise training rather than açaí fruit pulp consumption or a combination of both enhances the hepatic oxidative and inflammatory status ofApoE^− / −mice.

This study aims to analyze the effects of resisted, aerobic, and combined exercises on omentin levels in visceral adipose tissue and muscle of rats with experimental diabetes to verify whether these adipokines are related to the glucose pathway and inflammation process in this model. Male Wistar rats received a high-fat diet for 4 weeks and a low dose of streptozotocin (35 mg/kg) to induce experimental diabetes. After inducing diabetes, the animals were divided into 4 experimental groups (n = 10): diabetic control (C); resistance training (RT); aerobic training (AT); and combined training (CT). The groups were exercised for 12 weeks, 3 times/week, where: RT means the stair climbing protocol until exhaustion; AT is the 30 min/day reaching 20 m/min protocol, and CT is the combination of RT and AT. The AT group showed reduced retroperitoneal and mesenteric adipose tissue and abdominal fat deposits. Our study also showed a possible control of blood glucose, as well as decreased Interleukin 6 (IL-6) and C-reactive protein, increased circulating adiponectin and increased omentin in visceral adipose tissue. In addition, the AT group affected the glucose pathway by stimulating phosphorylation of Akt in muscle tissue. Omentin also showed a strong positive correlation with adiponectin and a moderate negative correlation with IL-6. Thus, our findings indicated that omentin in type 2 diabetes is changed by AT. Furthermore, increased omentin levels had a close association with the glucose pathway by stimulating phosphorylation of Akt in muscle tissue and with IL-6 in serum, suggesting that omentin is likely to have anti-inflammatory and protective action in experimental diabetes.

Purpose: Nanoparticles are resources of advanced nanotechnology being present in several products. Titanium dioxide nanoparticles are among the five most widely used NP currently expanding their benefits from the oil industry to the areas of diagnostic medicine due to their properties and small size. However, its impact on human health is still controversial in the literature. We aimed to evaluate the cytotoxicity of a new titanium NP functionalized with sodium carboxylic ligand (COOH⁻Na⁺) in human keratinocytes (HaCaT) and human fibroblasts (HDFn). Methods: The physical-chemical characterization was performed by the transmission electron microscopy (TEM), dynamic light scattering (DLS) and zeta potential techniques, respectively. MTT and LDH assays were used to assess cytotoxicity and cell membrane damage respectively, ELISA to identify the inflammatory profile and, reactive oxygen species assay and cytometry to detect reactive oxygen species and their relationship with apoptosis/necrosis mechanisms. Results: The results demonstrated a decrease in cell viability at the highest concentrations tested for both cell lines, but no change in LDH release was detected for the HaCaT. The cell membrane damage was found only at 100.0 μg/mL for the HDFn. It was demonstrated that cytotoxicity in the highest concentrations evaluated for both cell lines for the 72 h period. The HDFn showed damage to the cell membrane at a concentration of 100 μg/mL followed by a significant increase in reactive oxygen species production. No inflammatory profile was detected. The HaCaT showed apoptosis when exposed to the highest concentration evaluated and HDFn showed both apoptosis and necrosis for the same concentration. Conclusion: Thus, it is possible to conclude that the cytotoxicity mechanism differs according to the cell type evaluated, with HDFn being the most sensitive line in this case, and this mechanism can be defined in a dose and time dependent manner, since the highest concentrations also triggered death cell.