scholarly journals Effects of Photoperiod Change on Melatonin Secretion, Immune Function and Antioxidant Status of Cashmere Goats

Animals ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 766 ◽  
Author(s):  
Mao ◽  
Xu ◽  
Shi ◽  
Guo ◽  
Jin ◽  
...  

The photoperiod affects animals’ secretion of hormones, especially melatonin (MLT), which is involved in the regulation of the immune function and antioxidant status. The present experiment was conducted to study the effects of the photoperiod on MLT secretion, immune function, antioxidant status and related gene expression in goats. Eighteen adult female cashmere goats were randomly divided into three photoperiod groups: the control group (CG: natural photoperiod); the short-day photoperiod group (SDPP group: 8 h light; 16 h dark) and the shortening-day photoperiod group (SIPP group: lighting time shortened gradually from 16 h/d to 8 h/d). The experiment lasted for 60 days. The results showed that SDPP increased MLT concentration in serum at day 30 of the experiment (p < 0.05), but SIPP increased it at day 60 (p < 0.05). The activity of total superoxide dismutase (T-SOD), glutathione peroxidase (GPx) and catalase (CAT) increased (p < 0.05), and malondialdehyde (MDA) concentration decreased (p < 0.05) at day 30 in SDPP; no significant effects of SIPP were observed at day 30. Both SDPP and SIPP goats had higher activities of T-SOD, GPx and CAT (p < 0.05) at day 60. The concentration of immunoglobulin G (IgG), interleukin 1β (IL-1β) and interleukin 2 (IL-2) increased in SDPP (p < 0.05) at day 30. Both SDPP and SIPP raised the concentration of IgG, IL-1β and IL-2 at day 60 (p < 0.05). For the relative gene expression, the SDPP improved the gene expression of SOD1, CAT, GPx4, nuclear factor erythroid-2-related factor 2(Nrf2), IL-1β, IL-2 and tumor necrosis factor-α (TNF-α) (p < 0.05) in blood leukocytes at day 30. In addition, at day 60, goats in the SDPP group had a higher gene expression of CAT, GPx4, IL-1β and IL-2 (p < 0.05). Goats in SIPP had significantly higher gene expression of SOD1, CAT, GPx4, Nrf2, TNFα, IL-1β and IL-2 (p < 0.05) than those in CG. These results indicated that SDPP and SIPP could secrete more MLT and then improve the immune function and antioxidant status of the goats.

2020 ◽  
Vol 22 (4) ◽  
pp. 665-674
Author(s):  
L. V. Gankovskaya ◽  
L. V. Stakhovskaya ◽  
V. V. Grechenko ◽  
E. A. Koltsova ◽  
O. S. Uvarova ◽  
...  

Pathogenesis of ischemic stroke  is actively  involved  in the  system  of innate immunity. Under conditions of cerebral  ischemia, a number of biologically  active  substances are  released  that  interact with innate immunity receptors, in particular TLR2  and  TLR4, which  exacerbate inflammation in brain  tissue. Identification of predictor markers  at the level of the innate immunity system may foresee the clinical course of ischemic stroke and ensure timely treatment. Our objective was to study expression of TLR2 and TLR4 receptors in peripheral blood leukocytes  in patients with ischemic stroke in the dynamics of the disease. 27 people  were included in the study. The main  group consisted of patients with ischemic stroke of varying severity (n = 19). Patients of the main  group were divided into two subgroups:  with an NIHSS index value of < 10 (n = 10) and > 10 (n = 9). The control group included healthy  donors  with no history  of acute  and chronic inflammatory diseases (n = 8). Peripheral blood  leukocytes  were used as the  test material. To determine expression  of the TLR2  and TLR4  genes, RT-PCR in real time was used. Surface  expression  of TLRs was determined by flow cytometry. A study of the TLR2 and TLR4 gene expression showed that on the 1st, 3rd  and 7th  day post-stroke, the TLR4 gene expression  in patients was significantly  increased, when compared to the control group (p < 0.01), whereas TLR2 gene expression on the 3rd  day of the disease was not statistically different from the control group. A study of surface expression  of receptors showed that the average TLR2 fluorescence intensity on the patients’ peripheral blood monocytes was significantly  increased on the 1st  and 3rd  day of disease when compared to the control group.  The  surface  expression  of TLR4  on monocytes has a statistically significant  increase  only on day 7. Assessment  of surface expression  of TLRs in subgroups  with different  severity values by NIHSS showed that  patients with a NIHSS index > 10 had a significantly  higher  level of surface of TLR2  expression  over the observation period, while the largest difference in TLR4  expression  in the subgroups  was observed  on the 1st day of the disease (p < 0.05). Patients with ischemic stroke showed an increase  in TLR2 and TLR4 expression at the gene and protein level, compared to healthy  donors. These indices can be considered possible predictors for clinical  prognosis  of ischemic stroke.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Vanesa Palau ◽  
Bramasta Nugraha ◽  
Maximilian Emmert ◽  
Simon Hoerstrup ◽  
Julio Pascual Santos ◽  
...  

Abstract Background and Aims ADAM17 is a disintegrin and metalloproteinase initially described to cleave the tumor necrosis factor α (TNFα). Currently, it is known that it can also release ectodomains of a diverse variety of molecules such as, transforming growth factor α (TGFα), L-selectin, and angiotensin-converting enzyme 2 (ACE2). It has been shown that ADAM17 protein expression increases in kidney mesangial cells after incubation with high glucose media mimicking what has been observed in diabetic patients and experimental models of diabetic nephropathy. We now studied the effect ADAM17 deletion on human kidney cells (HKC-8) in a 3D spheroids in vitro cell culture incubated with high glucose, low glucose and mannitol medium resembling the in vivo human kidney diabetic environment. Method ADAM17 deletion was performed using the CRISPR/Cas9 technology. HKC8 cells grew inside a RGD-functionalized dextran hydrogel to obtain 3D spheroids. 13 days post-seeding, the spheroids were incubated with 35mM of D-glucose (HG), 5mM of D-glucose (LG) or 35mM of mannitol as osmotic control for 6h, 24h or 72h. The quality of the established 3D cell culture of mature HKC-8 spheroids was assessed by Aquoporin-1 and Glut-1 staining. After incubations quantitative-PCR analyses were performed for fibrotic and inflammatory markers. Immunofluorescence for fibrotic markers was performed on HKC-8 spheroids incubated for 72h. Results High glucose (HG) medium induced CCL5 gene expression on wild-type HKC-8 spheroids after 6h and 24h of incubation in comparison with the control group. Interestingly, in the ADAM17-deleted spheroids, CCL5 gene expression maintained similar to control after 6h of incubation with HG medium and tended to decrease after 24h of incubation in comparison with the wild-type. Collagen IV gene expression was increased in the wild-type spheroids incubated with HG in comparison with the control group. In ADAM17-deleted spheroids, Collagen IV gene expression was significantly decreased in the cells incubated with HG in comparison with the wild-type cells incubated with HG. HG increased the expression of α-SMA, fibronectin and Collagen IV in wild-type spheroids. Adam17 deletion blocked the increase of α-SMA, fibronectin and Collagen IV expression compared with wild-type cells after 72h of incubation. Conclusion ADAM17 blockade protects against fibrosis and inflammation in human kidney tubular spheroids under high glucose.


2021 ◽  
Vol 15 (5) ◽  
pp. 1551-1563
Author(s):  
E. Azizi ◽  
M. Hosseinzadeh ◽  
P. Vahdatian ◽  
A. Adibi ◽  
A. Azizifar ◽  
...  

Background: Schizophrenia is a mental disorder characterized by distortions in thinking, perception, emotions, language, self-sense, and behavior. Recent research suggests that Reactive Oxygen Species (ROS) are involved in the pathophysiology of schizophrenia. Studies have also shown the increased plasma and serum levels of the Trx1 molecule in schizophrenia patients. In the present study, the researchers compared the expression levels of Trx1 mRNA in peripheral blood leukocytes of Iranian schizophrenia patients compared to healthy controls. Methods: First-episode patients (n=35) who met DSM-IV criteria for schizophrenia were recruited from patients referred to psychiatrists in the city of Ilam and Farabi Hospital in Kermanshah. Healthy people were also selected by recruiting people who, according to a psychiatrist, did not have any mental illness. Diagnoses were made for each patient by two independent experienced psychiatrists and confirmed by the Structured Clinical Interview for DSM-IV (SCID). Patients were treated with risperidone for three months and then compared with thirty- five healthy volunteers. Patients were sampled before and after treatment and then by RNA Extraction and DNA synthesis, Trx1 gene expression was performed by real-time PCR method. Results: Comparison of Trx1 gene expression in PBMCs of schizophrenic patients before and after treatment with the control group showed that the expression of Trx1 gene of the “before” treatment group was significantly increased compared with that of the control group (P= 0.0007). Also, Trx1 gene expression in PBMCs of “before” and “after “groups showed that Trx1 gene expression of “after” group was significantly decreased compared to the “before” group (P= 0.014). These results showed that the mean of positive, negative, and general psychopathology was reduced significantly in schizophrenic patients before and after treatment in all three cases (P <0.001). Conclusion: the expression of TRX in PBMCs of schizophrenic patients decreased after risperidone treatment. This reduction of expression was statistically significant and indicates the possible effect of risperidone on the expression of the TRX gene in PBMCs of these patients and decreased gene expression is associated with reduced symptoms. Confirmation of the achievement of this study requires further research. Key words: Schizophrenia, Thioredoxin, Risperidone


2021 ◽  
Vol 19 (12) ◽  
pp. 2639-2644
Author(s):  
Zhongwen Sun ◽  
Libo Sun ◽  
Wenwen Li

Purpose: To investigate the hepatoprotective role of ganoderic acid A (GAA) on liver cancer induced by diethylnitrosamine (DEN) via Nrf-2/HO-1/NF-κB signal pathway in mice. Methods: Sixty male C57BL/6J mice were randomly divided into 4 groups: (1) control group, (2) DEN (25 mg/kg) group, (3) GAA (20 mg/kg) + DEN group, (4) GAA (40 mg/kg) + DEN group. The protective effect of GAA on liver was evaluated by determining malondialdehyde (MDA), superoxide dismutase (SOD), inflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the expression of heme oxygenase-1 (HO-1), nuclear factor erythroid- 2-related factor-2 (Nrf-2), IκBα, p-IκBα, p65, p-p65, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in serum. Results: The results demonstrate that GAA treatment significantly suppressed the generation of MDA, proinflammatory cytokines, and restored the activity of SOD in the serum of DEN-induced liver cancer in mice. Western blots analysis revealed that GAA significantly restored Nrf-2/HO-1/NF-κB signal pathwayrelated protein levels in DEN-induced mice liver cancer model. Conclusion: This research reveals the anticancer activity of GAA in liver tissue, and suggests that GAA counters DEN-induced liver  cancer through Nrf-2/HO-1/NF-κB signal pathway. Keywords: Ganoderic acid A, Nrf-2/HO-1/NF-κB pathway, Liver cancer, MDA, GAPDH, SOD


2022 ◽  
Vol 22 ◽  
Author(s):  
Moustafa M. Mohamed ◽  
Ahmed M. M. Okasha ◽  
Amany H. Abdel Naiem ◽  
Reham F. Mohamed ◽  
Sayed F. Abdelwahab ◽  
...  

Background: Autoimmune hepatitis (AIH) is an inflammatory liver disease which is characterized histologically by interface hepatitis, biochemically by elevated transaminase levels, and serologically by the presence of autoantibodies. Toll-like receptor (TLR)-4 is a TLR family member that, upon activation in hepatocytes, initiates a cascade of events. Interleukin-2 (IL-2) and tumour necrosis factor-α (TNF-α) are potent inflammatory cytokines secreted in AIH playing an important role in the early development of inflammation, and hepatocyte damage. Objective: This study examined cyclosporine role in AIH and tried to illustrate its actions on altered hepatic function in silica-induced AIH model. Methods: AIH was induced in Wester rats using Sodium Silicate. The rats were divided into four groups: control group, Silica-AIH group, cyclosporine-treated group, and prevention group. TLR-4, and IL-2 mRNA expression in liver tissues was tested by RT-PCR. Results: AIH was associated with up-regulation of liver enzymes, IL-2, and TLR-4 gene expression while cyclosporine significantly down-regulated the expression of both. The relative quantity of TLR-4 mRNA was 1±0, 13.57±1.91, 4±0.38, and 2±0 in the control, AIH, cyclosporine, and prevention groups, respectively (p<0.001). Also, the relative quantity of IL-2 mRNA was 1±0, 14.79±1.42, 7.07±0.96, and 3.4±0.55 in the same groups, respectively (p<0.001). Additionally, immuno-histochemical staining for TNF-α in liver sections was increased in the silica-AIH group but it was decreased in the cyclosporine-treated and prevention groups. Conclusion: This study advocates a therapeutic role of cyclosporine in treating immune-mediated hepatic diseases. Cyclosporine improves histological alterations in the liver and inhibits the production of proinflammatory cytokines.


2018 ◽  
Vol 19 (9) ◽  
pp. 2549 ◽  
Author(s):  
Luisa Brandt ◽  
Susanna Schubert ◽  
Patrick Scheibe ◽  
Walter Brehm ◽  
Jan Franzen ◽  
...  

Transplantation of multipotent mesenchymal progenitor cells is a valuable option for treating tendon disease. Tenogenic differentiation leading to cell replacement and subsequent matrix modulation may contribute to the regenerative effects of these cells, but it is unclear whether this occurs in the inflammatory environment of acute tendon disease. Equine adipose-derived stromal cells (ASC) were cultured as monolayers or on decellularized tendon scaffolds in static or dynamic conditions, the latter represented by cyclic stretching. The impact of different inflammatory conditions, as represented by supplementation with interleukin-1β and/or tumor necrosis factor-α or by co-culture with allogeneic peripheral blood leukocytes, on ASC functional properties was investigated. High cytokine concentrations increased ASC proliferation and osteogenic differentiation, but decreased chondrogenic differentiation and ASC viability in scaffold culture, as well as tendon scaffold repopulation, and strongly influenced musculoskeletal gene expression. Effects regarding the latter differed between the monolayer and scaffold cultures. Leukocytes rather decreased ASC proliferation, but had similar effects on viability and musculoskeletal gene expression. This included decreased expression of the tenogenic transcription factor scleraxis by an inflammatory environment throughout culture conditions. The data demonstrate that ASC tenogenic properties are compromised in an inflammatory environment, with relevance to their possible mechanisms of action in acute tendon disease.


2003 ◽  
Vol 284 (2) ◽  
pp. C415-C421 ◽  
Author(s):  
Rocio Rodriguez-Melendez ◽  
Gabriela Camporeale ◽  
Jacob B. Griffin ◽  
Janos Zempleni

Biotin has been credited with having beneficial effects on immune function despite observations that biotin supplementation causes decreased secretion of interleukin-2. Here this paradox was addressed by determining whether receptor-dependent internalization of interleukin-2 by immune cells depends on biotin. Theoretically, this would be consistent with both decreased net secretion of interleukin-2 by biotin-supplemented cells (causing increased endocytosis) and beneficial effects of biotin on immune function (causing increased receptor signaling). Jurkat cells were cultured in biotin-defined media (25, 250, or 10,000 pM). Secretion of interleukin-2 correlated negatively with biotin supply, but transcriptional activity of the interleukin-2 gene correlated positively with biotin supply, suggesting that decreased secretion of interleukin-2 by biotin-supplemented cells was not caused by decreased gene expression. Expression of the interleukin-2 receptor-γ gene was greater at 10,000 pM than 25 pM biotin, mediating increased endocytosis of interleukin-2 in biotin-supplemented medium. Inhibition of endocytosis by genistein and overexpression of interleukin-2 receptor-γ abolished the effect of biotin. These findings suggest that endocytosis of interleukin-2 depends on biotin.


Author(s):  
Ahmad Hamta ◽  
Fatemeh Hajihassani

Background: Cervical cancer (CC) is one of the most common malignant tumors in women, which has been diagnosed as fourth cancer in females worldwide. In addition to human papillomavirus (HPV), genetic factors, including altered expression of some microRNAs and mutations in tumor necrosis factor α (TNF-α) gene, are involved in this cancer. Objectives: This study aimed to investigate the rs11614913 polymorphism from the miRNA196a gene and its association with the expression of the TNF-α gene in cervical cancer for early diagnosis and treatment. Methods: In this study, 52 samples of pre-cancerous and cancerous lesions, and 50 tissue samples were collected from healthy subjects in an Iranian population. DNA was extracted from the samples, and rs11614913 polymorphism of the miRNA196a gene was investigated by PCR. RNA was extracted from the samples, and the expression of the miRNA196a and TNF-α genes were evaluated. Finally, for data analysis, Epi Info software version 7.1.3.10 and MedCalc Version 19.2.0 were used. Results: The frequency of CC, TC, and TT genotypes from rs11614913 polymorphism of miRNA196a gene was 0.58, 0.34, and 0.08, respectively, but in the healthy group it was 0.36, 0.46, and 0.18, respectively. The results also showed that the expression of miRNA196a and TNF-α genes in the patient group was higher than the control group. Conclusions: Based on the results of this study, a significant correlation was found between CC genotype and rs11614913 polymorphism of miRNA196a gene and TNF-α gene expression in the cervical cancer sample. Therefore, investigating these factors in patients with cervical cancer may be helpful.


Tumor Biology ◽  
2019 ◽  
Vol 41 (4) ◽  
pp. 101042831984304 ◽  
Author(s):  
Demétrius Eduardo Germini ◽  
Maria Isete Fares Franco ◽  
Fernando Luiz Affonso Fonseca ◽  
Flávia de Sousa Gehrke ◽  
Beatriz da Costa Aguiar Alves Reis ◽  
...  

Inflammation is an important etiological factor of colorectal carcinoma and may be related to colorectal carcinoma growth and proliferation. This study aimed to verify whether the presence of chronic inflammation represented by tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-10 gene expression is related to hMLH1, hMSH2, hMSH6, and PMS2 gene expression and the corresponding protein levels of these genes from the DNA repair system. A total of 83 patients were operated on for curative or palliative colorectal carcinoma. Expression of the inflammatory response genes tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-10 as well as expression of the hMLH1, hMSH2, hMSH6, and PMS2 genes of the DNA repair system (mismatch repair) and the expression levels of the corresponding mismatch repair proteins were measured in neoplastic tissue by reverse transcription polymerase chain reaction and immunohistochemistry, respectively. Associations were observed between hMSH6 mRNA expression and interleukin-2 mRNA expression (p = 0.026) as well as between hMLH1 and hMSH2 gene expression and tumor necrosis factor-α gene expression (p = 0.042). Higher tissue levels of interleukin-2 and tumor necrosis factor-α gene expression were associated with lower hMSH6, hMLH1, and hMSH2 gene expression.


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