Cytotoxic properties of hydroalcoholic extract on androgen unresponsive prostate cancer cells.

Androgen independent phase in prostate cancer (PCa) commonly limits the therapeutic efficacy. through its main active compound, α-thujone, appears to be an option, considering its anti-proliferative, anti-metastatic and pro-apoptotic effects on hepatocellular carcinoma. However, studies on PCa are limited.

Aqueous PM promotes lipid accumulation, classical macrophage polarisation and heat shock response.

Fine particulate matter (PM) is an air pollutant that enhances susceptibility to cardiovascular diseases. Macrophages are the first immune cells to encounter the inhaled particles and orchestrate an inflammatory response. Given their role in atherosclerosis development, we investigated whether aqueous PM could elicit atherogenic effects by polarising macrophages to a pro-oxidative and pro-inflammatory phenotype and enhancing foam cell formation.

Air pollution combined with high-fat feeding aggravates metabolic and cardiovascular diseases: A dangerous, oxidative, and immune-inflammatory association.

Unlabelled: Obesity and particulate air pollutant (PM) are important risk factors for cardiometabolic diseases. PM exacerbates insulin resistance and lipid ectopic deposition in obese animals. The inorganic fraction of PM the Residual Oil Fly Ash (ROFA), is related to cardiovascular events, by enhancing the generation of reactive species, inflammatory cytokines, and leukocyte activation.

The macrophage senescence hypothesis: the role of poor heat shock response in pulmonary inflammation and endothelial dysfunction following chronic exposure to air pollution.

Introduction: Cardiovascular diseases (CVD) have been associated with high exposure to fine particulate air pollutants (PM). Alveolar macrophages are the first defense against inhaled particles. As soon as they phagocytize the particles, they reach an inflammatory phenotype, which affects the surrounding cells and associates with CVD.

Moderate aerobic training is safe and improves glucose intolerance induced by the association of high fat diet and air pollution.

Obesity and exposure to fine particulate matter (PM) are risk factors for insulin resistance, to which physical exercise is the most powerful non-pharmacological strategy. However, public concern over whether exercise could be protective in a polluted environment exists. Therefore, evaluating the possible benefits of exercise in polluted conditions in different contexts (age, gender, and cardiometabolic health) is imperative.

Increased eHSP70-to-iHSP70 ratio in prediabetic and diabetic postmenopausal women: a biomarker of cardiometabolic risk.

Decreased estrogen levels in menopause are associated with anthropometric, metabolic, and inflammatory impairments, predisposing women to cardiometabolic risk factors such as diabetes. Menopause and type two diabetes (DM2) are marked by altered heat shock response (HSR), shown by decreased expression of the 70-kDa heat shock protein in the intracellular milieu (iHSP70). While iHSP70 plays an anti-inflammatory role, extracellular HSP70 (eHSP70) may mediate pro-inflammatory pathways and has been associated with insulin resistance in DM2.

HSP70 as a biomarker of the thin threshold between benefit and injury due to physical exercise when exposed to air pollution.

Physical exercise has acute and chronic effects on inflammatory balance, metabolic regulation, and redox status. Exercise-induced adaptations are mediated by enhanced 70-kDa heat shock protein (HSP70) levels and an improved heat shock response (HSR). Therefore, exercise could be useful against disease conditions [obesity, diabetes mellitus (DM), and exposure to atmospheric pollutants] marked by an impaired HSR.

Oxidative and Cellular Stress Markers in Postmenopause Women with Diabetes: The Impact of Years of Menopause.

Women live approximately one-third of their lives in postmenopause. Among postmenopausal women, type 2 diabetes mellitus (DM2) is one of the most prevalent chronic diseases. These conditions promote alterations in the oxidative, metabolic, and immune-inflammatory profiles marked by higher extracellular 72 kDa-heat shock protein (eHSP72).

Ovariectomy reduces the cardiac cytoprotection in rats exposed to particulate air pollutant.

Fine particulate matter (PM) has been considered a risk factor for cardiovascular diseases by inducing an oxidative and inflammatory phenotype. Besides, the reduction of 17β-estradiol (E2) levels during menopause is a natural risk for cardiovascular outcomes. During the E2 downfall, there is a high requirement of the 70-kDa heat shock proteins (HSP70), which present essential antioxidant, anti-inflammatory, and anti-senescence roles.

Ovariectomy enhances female rats' susceptibility to metabolic, oxidative, and heat shock response effects induced by a high-fat diet and fine particulate matter.

Obesity and exposure to fine particulate matter (air pollutant PM) are important risk factors for metabolic and cardiovascular diseases. They are also related to early menopause. The reduction of 17β-estradiol (E2) levels during female climacteric, marked by menopause, is of significant concern because of its imminent influence on metabolism, redox and inflammatory status.

The association of subchronic exposure to low concentration of PM and high-fat diet potentiates glucose intolerance development, by impairing adipose tissue antioxidant defense and eHSP72 levels.

The subchronic exposure to fine particulate matter (PM) and high-fat diet (HFD) consumption lead to glucose intolerance by different mechanisms involving oxidative stress and inflammation. Under stressful conditions, the cells exert a heat shock response (HSR), by releasing the 72-kDa heat shock proteins (eHSP72), fundamental chaperones. The depletion of the HSR can exacerbate the chronic inflammation.

Chaperone duality: the role of extracellular and intracellular HSP70 as a biomarker of endothelial dysfunction in the development of atherosclerosis.

The 70-kDa heat shock proteins (HSP70) may provide relevant information about the endothelial dysfunction in cardiovascular diseases. Located in the intracellular milieu (iHSP70), they are essential chaperones that inhibit nuclear factor kappa B activation, stimulate nitric oxide production and superoxide dismutase activity, and inhibit apoptosis. However, under stressful conditions, HSP70 can be released into the extracellular medium (eHSP70) and act as an inflammatory mediator.

Chronic heat treatment positively impacts metabolic profile of ovariectomized rats: association with heat shock response pathways.

Low estrogen levels may predispose women to increased bodyweight and dyslipidemia. Previous studies from our laboratory suggest an involvement of depressed heat shock response (HSR) in this scenario because estrogen potently stimulates HSR. As heat treatment induces the expression of the anti-inflammatory heat shock proteins of the 70-kDa family (HSP70) and its accompanying HSR, we aimed to investigate whether chronic heat treatment promotes beneficial effects on biometric, lipid profile, oxidative stress, and HSR in ovariectomized rats.

Ovariectomy predisposes female rats to fine particulate matter exposure's effects by altering metabolic, oxidative, pro-inflammatory, and heat-shock protein levels.

The reduction of estrogen levels, as a result of menopause, is associated with the development of metabolic diseases caused by alterations in oxidative stress (OS), inflammatory biomarkers, and 70-kDa heat-shock protein (HSP70) expression. Additionally, exposure to fine particulate matter air pollution modifies liver OS levels and predisposes organisms to metabolic diseases, such as type 2 diabetes (T2DM). We investigated whether ovariectomy affects hepatic tissue and alters glucose metabolism in female rats exposed to particulate air pollution.

Effects of High-Fat Diet on eHSP72 and Extra-to-Intracellular HSP70 Levels in Mice Submitted to Exercise under Exposure to Fine Particulate Matter.

Obesity, air pollution, and exercise induce alterations in the heat shock response (HSR), in both intracellular 70 kDa heat shock proteins (iHSP70) and the plasmatic extracellular form (eHSP72). Extra-to-intracellular HSP70 ratio (H-index = eHSP70/iHSP70 ratio) represents a candidate biomarker of subclinical health status. This study investigated the effects of moderate- and high-intensity exercise in the HSR and oxidative stress parameters, in obese mice exposed to fine particulate matter (PM).

Exercise Training under Exposure to Low Levels of Fine Particulate Matter: Effects on Heart Oxidative Stress and Extra-to-Intracellular HSP70 Ratio.

Fine particulate matter (PM) promotes heart oxidative stress (OS) and evokes anti-inflammatory responses observed by increased intracellular 70 kDa heat shock proteins (iHSP70). Furthermore, PM increases the levels of these proteins in extracellular fluids (eHSP70), which have proinflammatory roles. We investigated whether moderate and high intensity training under exposure to low levels of PM modifies heart OS and the eHSP70 to iHSP70 ratio (H-index), a biomarker of inflammatory status.