CD11c is a member of the β2‐integrin family typically used to define myeloid dendritic cells (DCs). Recent reports identify CD11c‐expressing CD8+ T cells as a new subset of CD8+ regulatory T cells (Treg). Evidence exists that CD11c+CD8+ T cells may exert their effector or regulatory functions under different conditions. To date, no studies have addressed the frequency of CD11c+ T cells in cancer. Limited evidence exists in terms of expression of immune‐checkpoint receptors, programmed cell death protein 1 (PD‐1) and T‐lymphocyte‐associated antigen 4 (CTLA‐4), as well as forkhead box P3 (Foxp3) in mouse lymphoid organs. Here, we have assessed CD11c+CD8+ and CD11c+CD4+ T cells, Foxp3, PD‐1, and CTLA‐4 expressing CD4+ T cells and CD8+ T cells in different tissues from three groups of male BALB/c mice—young, mature, and those with colorectal cancer (CRC). Analysis of CD3+CD11c+ T cells in the bone marrow (BM), spleen, and lymph nodes (LN) in each group showed a higher percentage of CD3+CD11c+ T cells in the BM from all groups and in the lymphoid organs of the cancer group compared with the young and mature groups. CD4low and CD4high cell fractions in mice BM have different expression patterns for Foxp3 and CTLA‐4. We have observed a higher frequency of CD8+PD‐1+ T cells in the BM, spleen, and LN of CRC mice compared with normal mice. T‐cell exhaustion is associated with inhibitory receptor PD‐1. According to the regulatory roles of CD11c expression in CD8+ T cells, we have proposed that the elevated percentage of CD11c, Foxp3, CTLA‐4, and PD‐1 expressing T cells were associated with immune response dysregulation in CRC.
Background and objective: Proper exercise and nutrition can help prevent bone disorders in old age, therefore present study aimed to investigate the effects of high intensity interval training (HIIT) with genistein (Ge) on biomechanical properties of femur bone in elderly female rats. Methods: In this experimental study, 40 elderly female rats with mean age of 18-24 months and mean weight of 220.15±15.28 g were divided into five groups of eight rats including: 1) control (C), 2) sham (Sh), 3) HIIT, 4) HIIT + Ge, and 5) Ge. During eight weeks groups 3 and 4 performed HIIT for three sessions per week with an intensity of 90 to 95% of maximum oxygen consumption (VO2max) in high intensity intervals and 40 to 45% VO2max in low intensity intervals and groups 4 and 5 received 60 mg/kg/day Ge peritoneally. Maximum bending strength (Fmax) measured with three-point bending test and serum levels of calcium (Ca) and phosphorus were measured by o-Cresolphthalein and molybdate methods, respectively. Shapiro-Wilk, one way ANOVA with Tukey's posthoc tests were used for analysis of data (P≤0.05). Results: HIIT (P=0.02), Ge (P=0.001) and HIIT+Ge (P=0.001) significantly increased Fmax also Ge (P=0.04) and HIIT+Ge (P=0.03) had more favorable effect on increasing Fmax compare to HIIT nevertheless HIIT, Ge and HIIT+Ge had not significant effect on Ca and phosphorus (P≥0.05). Conclusion: Although HIIT and Ge alone can enhance Fmax in femur of elderly female rats, nevertheless HIIT+Ge has more favorable effect on increase of Fmax compare to HIIT.
Background mTORC1 marker pathway is one of the crucial pathways for the regulation of transcription level and an essential route involved in protein synthesis in skeletal muscles. Objective This study aimed to investigate the effect of endurance training on mTORC1 marker pathway in soleus muscle of type 2 diabetic rats. Methods In this experimental study, 16 Sprague-Dawley male rats (Mean±SD weight: 270±20g) were obtained. After induction of diabetes (by streptozotocin administration), the rats were randomly assigned into two groups: endurance training and control. The exercise training was administered to the experimental group performed 4 days a week for 8 weeks, while the control group did not receive any training program. The study proteins were measured using western blot method. The Independent t-test analyzed the obtained data. Findings A significant change was not observed in the total content of Akt1 proteins, P70S6K1, 4E-BP1, and P70S6K1 phosphorylation content in the experimental group compared to the control group, but the total protein content of mTOR, the phosphorylation form of Akt1 proteins, and 4E-BP1 was significantly higher in the experimental group compared to the control group. Conclusion Eight weeks of endurance training can activate the Akt1/mTOR/4E-BP1 pathway in the mTORC1. Therefore, with regard to muscle atrophy in type 2 diabetic patients, endurance training can activate the mTORC1 marker pathway to regulate the transcription genes and subsequently, the expression of proteins.
Background The FOXO3a/Beclin-1 pathway is an important pathway in autophagy that can be impaired in diabetic patients who are prone to cardiomyopathy. Objective The aim of this study was to investigate the effect of an 8-week endurance training program on the content of FOXO3a and Beclin-1 proteins in the heart muscle tissue of rats with type 2 diabetes. Methods This experimental study was conducted on 12 male two-month-old Sprague Dawley rats with a mean weight of 270±20 g. After diabetic induction by streptozotocin and nicotinamide, rats were randomly assigned into two groups of diabetic-exercise (n=6) and diabetic-control (n=6). The diabeticexercise group received intervention 4 days per week, each session for 42 minutes at a speed of 10-30 m/m for 8 weeks, while the control group received no any training program. The rats did not receive any insulin treatment during the study. Collected data were analyzed using independent t-test at a significance level of P≤0.05. Findings No significant changes were observed in the content of FOXO3a (P=0.12) and Beclin-1 (P=0.34) proteins in the training group compared to the control group after intervention. Conclusion The endurance training can not affect the content of FOXO3a and Beclin-1 proteins. Therefore, it seems that endurance training may not affect autophagy signaling in the heart muscle of type 2 diabetic patients.
Introduction: Mitochondrial disorders play an essential role in reducing the health, infes tation, and progression of aging. The SIRT3 in mitochondria coordinates many mitochondrial biological aspects that are important in aging. Moreover, it alters directly the activity of many metabolic enzymes. Exercise has been able to enhance SIRT3 protein's expression and improve antioxidant function and neuroprotection. Resveratrol acts as a modulator of SIRT3 and has anti-aging and neuroprotective effects. The aim of this s tudy was to determine the effect of HIIT swimming activity and resveratrol supplementation on SIRT3 levels in the frontal lobe among older rats. Materials and Methods: Thirty rats were randomly divided into 5 groups; control (C), solvent (S), supplement (R), HIIT exercise (EX), HIIT exercise, and supplement (EXR)). The EX group performed HIIT swimming training for six weeks. Group C rats did not practice. Group R rats received only resveratrol supplementation. Rats in the EXR group performed HIIT swimming exercises with resveratrol. Group S received the only solvent. The SIRT3 protein levels were assessed frontal lobe of the rats. Results: A significant increase in SIRT3 protein was observed in group R, EX, and EXR groups compared to the control group. In addition, there was a subs tantial difference between the mean values of SIRT3 protein among the three groups. SIRT3 levels in the EX and EXR groups were significantly greater compared to the R group. Conclusion: Increasing the amount of SIRT3 in the response of HIIT swimming training in older rats indicating the involvement of this protein in metabolic pathways, antioxidant defense, and neuroprotection. In addition to metabolic tissues, this process occurs in the frontal lobe of the brain.n
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.