Allice Santos Cruz Veras

Cancer cachexia, characterized by severe body weight loss, negatively affects patient quality of life and survival. Although moderate exercise benefits healthy and chronically ill individuals, and the effect of exercise in cachexia generally appears beneficial, conflicting results have been reported in cancer-associated cachexia. This study examined the effects of moderate aerobic exercise in a rat cancer model, focusing on molecular crosstalk among tumors, serum, and skeletal muscle. Male Sprague-Dawley rats were divided into Non-Cancer, Cancer, and Cancer + Exercise (Ex) groups. Cancer was induced with an intraperitoneal injection of 7,12-dimethylbenz[a]anthracene (DMBA), and the Cancer + Ex group completed an eight-week treadmill regimen. Tibialis anterior muscle, serum, and tumor tissues were analyzed by RNA sequencing. DMBA injection produced sarcoma-like tumors, reduced body weight, elevated inflammatory mediators, and activated muscle atrophy genes (Fbxo32). Exercise led to progressive intolerance, further weight loss, lower muscle mass, and larger tumors. Transcriptomic profiling revealed exacerbated cachexia signatures and suppressed energy metabolism genes in exercised cancer rats. Bioinformatic analysis of serum proteins and tissue transcriptomes identified enhanced chemokine-receptor signaling, including pro-tumorigenic (CXCL6_CXCR2) and pro-cachexia (CCL19_CXCR3, CCL5_CCR3, CXCL11_CXCR3) interactions. These findings suggest that in a pro-inflammatory cancer context, late-onset moderate exercise may worsen cachexia and stimulate tumor progression. Thus, exercise protocols should be cautiously tailored in cancer settings.

Hypertension is an age-related pathology that causes a decline in the function of all organ systems, including the reproductive system, due to its association with increased oxidative stress and inflammation. The inflammatory cytokine levels increase as a result of hypertension and cause inflammation and tissue injury. Although high-intensity interval training (HIIT) has shown promise as a nondrug treatment for hypertensive individuals, its effects on the reproductive system of hypertensive individuals remain unknown. The aim of this study was to investigate the effects of HIIT on plasma hormone concentrations and the expression of inflammatory mediators in the testes of spontaneously hypertensive rats (SHRs). Male SHRs were divided into 2 groups: SHR (control, n=8) and HIIT (SHRs subjected to HIIT on a treadmill for 8 weeks, n=9) groups. The expression of inflammatory mediators (TNFα and IL-6) in the testes and testosterone, prolactin, and corticosterone concentrations in plasma were measured. No difference in TNFα expression was found between the groups. The groups also showed no significant differences in hormone levels. However, SHRs that underwent HIIT showed lower immunostaining for IL-6 in their testes than did SHRs that did not undergo HIIT training (P < 0.05) and the HIIT group presented lower lower systolic blood pressure than did the SHR group. We concluded that HIIT for two months reduces the BSP and IL-6 levels in the testes of hypertensive rats.

Arterial hypertension promotes urological complications by modifying the functional capacity of the urinary bladder. On the other hand, physical exercise has been suggested as a nonpharmacological tool to improve blood pressure regulation. High-intensity interval training (HIIT) can effectively increase peak oxygen consumption, body composition, physical fitness, and health-related characteristics of adults; however, its action on the urinary bladder is little discussed. In the present study, we verified the effect of HIIT on the modulation of the redox state, morphology, and inflammatory and apoptotic processes of the urinary bladder of hypertensive rats. Spontaneously hypertensive rats (SHR) were divided into two groups: SHR sedentary and SHR submitted to HIIT. Arterial hypertension promoted an increase in the plasma redox state, modified the volume of the urinary bladder, and increased collagen deposition in detrusor muscle. It was also possible to identify, in the sedentary SHR group, an increase in inflammatory markers such as IL-6 and TNF-α in the urinary bladder, as well as a reduction in BAX expression. However, in the HIIT group, reduced blood pressure levels were observed, together with an improvement in morphology, such as a decrease in collagen deposition. HIIT also regulated the proinflammatory response, promoting increases in IL-10 and BAX expressions and in the number of plasma antioxidant enzymes. The present work highlights the intracellular pathways involved with the oxidative and inflammatory capacity of the urinary bladder and the potential effect of HIIT on the regulation of the urothelium and detrusor muscle of hypertensive rats.

Guided bone regeneration (GBR) is a common practice in implantology, and it is necessary to use membranes in this process. The present study aimed to evaluate the osteopromotive principle of two porcine collagen membranes in critical-size defects at rats calvaria. Ninety-six Albinus Wistar rats were divided into BG (positive control), JS, CS, and CG (negative control) groups and were sacrificed at 7, 15, 30, and 60 days postoperatively. The samples were assessed by histological, histometric, immunohistochemical, and microtomographic analyses. More intense inflammatory profile was seen in the JS and CS groups (p < 0.05). At 60 days, the JS group showed a satisfactory osteopromotive behavior compared to BG (p = 0.193), while CS did not demonstrate the capacity to promote bone formation. At the immunohistochemical analysis, the CS showed mild labeling for osteocalcin (OC) and osteopontin (OP), the JS demonstrated mild to moderate for OC and OP and the BG demonstrated moderate to intense for OC and OP. The tridimensional analysis found the lowest average for the total volume of newly formed bone in the CS (84,901 mm²), compared to the BG (319,834 mm²) (p < 0.05). We conclude that the different thicknesses and treatment techniques of each membrane may interfere with its biological behavior.

Background: The prostatic effects induced by arterial hypertension is very controversial and its mechanism is unclear. High‐intensity interval training (HIIT) is an exercise considered to be hypotensive. The objective of this work was to investigate the molecular, biochemical, and morphological effects of 8 weeks of HIIT in the prostatic tissue of spontaneously hypertensive rats (SHR).Methods: Twenty male SHR rats, 51.4 weeks old, were used. The SHR animals were divided into two groups: spontaneously sedentary hypertensive and spontaneously hypertensive submitted to HIIT. We analyze androgens receptor and glucocorticoid receptors in the prostate. Still, we verify effects of the hypertension and HIIT on the physiopathology prostatic, for immunohistochemistry investigated BCL‐2, BAX, IGF‐1, FAS/CD95, data's inflammatory tumour necrosis factor α, nuclear factor kappa B and interleukin (IL)‐6, anti‐inflammatory IL‐10. The echocardiographic evaluation was performed at the baseline and after the training period.Results: Arterial hypertension promote high prostatic intraepithelial neoplasia incidence in the prostate, increases IGF‐1, BCL‐2 (p < 0.05), and inflammatory proteins (p < 0.05). Eight weeks of HIIT training reduced the arterial pressure and increase the concentration of tissue collagen and intracellular glycogen and showed a higher expression of BAX, FAS/CD95, and IL‐10 proteins (p < 0.05), coinciding with a lower incidence of lesions and lower prostate weight (p < 0.05) and reduction of the BCL‐2 and IGF‐1.Conclusion: Our data suggested that arterial hypertension suppressed apoptosis and increased damage prostatic. On other hand, HIIT promotes morphology and function improves in the prostatic environment, inhibited inflammation, and increased apoptosis.

Alcoholic injury can alter the hormonal signaling pathway and lead to glucose and lipid metabolism disorders. In this study, we investigated whether the strength training could exert protective effects against the alterations caused by ethanol consumption on prostatic metabolism. A UChB, ethanol‐preferring rats were used in this study. Strength training was conducted for 3 days per week for 13 weeks, rats performed jumps in water carrying a weight load strapped to their chests as part of a strength training protocol. The reduced alcohol consumption by strength training was accompanied by increased glucose, serum lipid profile, total protein levels, and reduced hormonal levels. The results of protein expression of prostatic tissues in the ethanol‐ and strength training‐treated groups indicated that “steroidal hormone receptors,” “fatty acid translocation,” and “cell regulation” were significantly different between ethanol‐ and strength training‐treated groups. Taken together, these findings show that strength training effectively ameliorated prostatic injuries in alcoholic rats at least partially by acting on lipids receptors and steroidal hormone receptors pathway, suggesting the strength training as a potential novel therapeutic strategy for treating prostate injuries caused by ethanol.

The protective effects of chronic moderate exercise-mediated autophagy include the prevention and treatment of several diseases and the extension of lifespan. In addition, physical exercise may impair cellular structures, requiring the action of the autophagy mechanism for clearance and renovation of damaged cellular components. For the first time, we investigated the adaptations on basal autophagy flux in vivo in mice’s liver, heart, and skeletal muscle tissues submitted to four different chronic exercise models: endurance, resistance, concurrent, and overtraining. Measuring the autophagy flux in vivo is crucial to access the functionality of the autophagy pathway since changes in this pathway can occur in more than five steps. Moreover, the responses of metabolic, performance, and functional parameters, as well as genes and proteins related to the autophagy pathway, were addressed. In summary, the regular exercise models exhibited normal/enhanced adaptations with reduced autophagy-related proteins in all tissues. On the other hand, the overtrained group presented higher expression of Sqstm1 and Bnip3 with negative morphological and physical performance adaptations for the liver and heart, respectively. The groups showed different adaptions in autophagy flux in skeletal muscle, suggesting the activation or inhibition of basal autophagy may not always be related to improvement or impairment of performance.

Our aim is to evaluate the effects of high-fat diet and strength training on ventral prostate health through investigations of rat prostate histology, endocrine modulation, and the expression of proliferative and apoptotic marker, including androgen receptors (AR), glucocorticoid receptors (GR), B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (BAX), Fas cell surface death receptor (Fas/CD95/Apo-1), and Nuclear Factor Kappa-B (NF-κB). Eighty Wistar rats were into one of four subgroups: control (CT), strength training (ST), high-fat diet consumption (HF), and high-fat diet consumption with strength training (HFT). Animals then underwent strength training and/or high-fat diet consumption for 8 or 12 weeks, after which animals were euthanized and markers of prostatic health were evaluated histologically and through immunolabeling. Our results indicate that physical strength training reduced the expression of the prostate cell proliferation marker Bcl-2 while increasing expression of the pro-apoptotic marker BAX, as well as increasing expression of AR and GR relevant in the Bcl-2 pathway. We conclude that a high-fat diet can alter hormone receptor levels and cell-cycle protein expression, thereby modifying prostatic homeostasis, and that strength training was able to reduce prostate damage induced by high-fat diet consumption.