scholarly journals Effect of antioxidant treatment with n-acetylcysteine and swimming on lipid expression of sebaceous glands in diabetic mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Geovane Ribeiro Santos ◽  
Marcelo Rodrigues Cunha ◽  
Eduardo José Caldeira ◽  
Ewerton Alexandre Galdeano ◽  
Raphael Cruz Seabra Prudente ◽  
...  

AbstractThe sebaceous gland (SG) is involved in different inflammatory, infectious and neoplastic processes of the skin and can be related to specific diseases, e.g., diabetes mellitus. Sometimes, the histological diagnosis requires complementary tests due to the ability of diseases to mimic other tumors. We evaluated the sebaceous gland density in Non-obese diabetic mice to analyze the N-acetylcystein effects and swimming exercise treatment in sebaceous glands healing, using specific staining in histochemistry and immunohistochemistry reactions in the identification of the lipid expression in the sebaceous gland. We investigated the intracytoplasmic lipid expression and analysis of gland density from SG in dorsal skin samples from the Non-obese diabetic (NOD mice) and diabetic animals submitted to antioxidant treatment and physical exercise. For histological analysis of the sebaceous glands, specific staining in histochemistry with sudan black and immunohistochemistry reaction with adipophilin were used in the evaluation. Statistical analysis showed significant proximity between the values of the control group and the diabetic group submitted to the swimming exercise (DS group) and similar values between the untreated diabetic group (UD group) and diabetic group treated with the antioxidant N-acetylcysteine (DNa group), which did not prevent possible differences where p < 0.01. Adipophilin (ADPH) immunohistochemistry permitted more intense lipid staining in SGs, the preservation of the SG in the control group, and a morphological deformed appearance in the UD and DNa groups. However, weak morphological recovery of the SG was observed in the DS-Na group, being more expressive in the DS group. In conclusion, the groups submitted to physical exercises showed better results in the recovery of the analyzed tissue, even being in the physiological conditions caused by spontaneous diabetes.

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 193
Author(s):  
Shiri Li ◽  
Nosratola D. Vaziri ◽  
Lourdes Swentek ◽  
Chie Takasu ◽  
Kelly Vo ◽  
...  

Oxidative stress plays critical roles in the pathogenesis of diabetes. This study tested the hypothesis that by protecting β-cells against oxidative stress and inflammation, an Nrf2 activator, dimethyl fumarate (DMF), may prevent or delay the onset of type 1 diabetes in non-obese diabetic (NOD) mice. Firstly, islet isolation was conducted to confirm the antioxidative effects of DMF oral administration on islet cells. Secondly, in a spontaneous diabetes model, DMF (25 mg/kg) was fed to mice once daily starting at the age of 8 weeks up to the age of 22 weeks. In a cyclophosphamide-induced accelerated diabetes model, DMF (25 mg/kg) was fed to mice twice daily for 2 weeks. In the islet isolation study, DMF administration improved the isolation yield, attenuated oxidative stress and enhanced GCLC and NQO1 expression in the islets. In the spontaneous model, DMF significantly reduced the onset of diabetes compared to the control group (25% vs. 54.2%). In the accelerated model, DMF reduced the onset of diabetes from 58.3% to 16.7%. The insulitis score in the islets of the DMF treatment group (1.6 ± 0.32) was significantly lower than in the control group (3.47 ± 0.21). The serum IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-9, IL-12p70, IFN-γ, TNF-α, MCP-1 and CXCL16 levels in the DMF-treated group were lower than in the control group. In conclusion, DMF may protect islet cells and reduce the incidence of autoimmune diabetes in NOD mice by attenuating insulitis and proinflammatory cytokine production.


2021 ◽  
Author(s):  
Jin Yuan Wang ◽  
Duo Ma ◽  
Min Luo ◽  
Yong-Peng Tan ◽  
Ou Zhong ◽  
...  

Abstract Diabetes mellitus (DM), a high incidence metabolic disease, is related to the impairment of male spermatogenic function. Spermidine (SPM), one of the biogenic amines, was identified from human seminal plasma and believed to have multiple pharmacological functions. However, there exists little evidence that reported SPM's effects on moderating diabetic male spermatogenic function. Thus, the objective of this study was to investigate the SPM's protective effects on testicular spermatogenic function in streptozotocin (STZ)-induced type 1 diabetic mice. Therefore, 40 mature male C57BL/6J mice male were divided into four main groups: the control group (n=10), the diabetic group (n=10), the 2.5 mg/kg SPM-treated diabetic group (n=10) and the 5 mg/kg SPM-treated diabetic group (n=10), which was given intraperitoneally for 8 weeks. The type 1 diabetic mice model was established by a single intraperitoneal injection of STZ 120 mg/kg. The results showed that, compare to the control group, the body and testis weight, as well the number of sperm were decreased, while the rate of sperm malformation was significantly increased in STZ-induced diabetic mice. Then the testicular morphology was observed, which showed that seminiferous tubule of testis were arranged in mess, the area and diameter of which was decreased, along with downregulated anti-apoptotic factor (Bcl-2) expression, and upregulated pro-apoptotic factor (Bax) expression in the testes. Furthermore, testicular genetic expression levels of Sertoli cells (SCs) markers (WT1, GATA4) and Vimentin detected that the pathological changes aggravated observably, such as the severity of tubule degeneration increased. Compared to the saline-treated DM mice, SPM treatment markedly improved testicular function, with an increment in the body and testis weight as well as sperm count. Pro-apoptotic factor (Bax) was down-regulated expression with the up-regulated expression of Bcl-2 and suppression of apoptosis in the testes. What’s more, expression of WT1, GATA4, Vimentin and the expressions of glycolytic rate-limiting enzyme genes (HK2, PKM2, LDHA) in diabetic testes were also upregulated by SPM supplement. The evidence derived from this study indicated that the SMP's positive effect on moderating spermatogenic disorder in T1DM mice's testis. This positive effect is delivered via promoting spermatogenic cell proliferation and participating in the glycolytic pathway's activation.


2020 ◽  
Vol 16 (8) ◽  
pp. 889-894 ◽  
Author(s):  
Mohammad Reza Alipour ◽  
Nasibeh Yousefzade ◽  
Fariba Mirzaei Bavil ◽  
Roya Naderi ◽  
Rafighe Ghiasi

Background: Obesity-induced chronic inflammation is a key component in the pathogenesis of insulin resistance and type-2 diabetes Objective: This study aimed to evaluate the effect of swimming exercise on pancreatic expression levels of inflammatory cytokines, miR-146a and NF-кB in type-2 diabetic male rats. Method: Twenty- eight male Wistar rats were divided into four groups: control (Con), exercise, diabetes and diabetic exercise (n = 7). Diabetes induction performed by the combination of high-fat diet (HFD, 4 weeks) and streptozotocin (35 mg/kg. ip). After induction of diabetes, the rats swam in the exercise groups for 12 weeks. Then, blood and tissue samples were collected. Result: Our results indicated a significant increase in expression levels of miR-146, NF-κB and inflammatory cytokines (IL-6, TNF-α, and IL-1β) while a significant decrease in pancreatic expression levels of TRAF6 and IRAK1 in diabetic group as compared to the control group. In contrast, swimming exercise resulted in a significant decrease in expression levels of miR-146a, NF-кB and inflammatory cytokines and a significant increase in expression levels of TRAF6 and IRAK1 in the exercise-diabetic group compared to the diabetic group. Conclusion: Our results indicated a significant increase in expression levels of miR-146, NF-κB and inflammatory cytokines (IL-6, TNF-α, and IL-1β) while a significant decrease in pancreatic expression levels of TRAF6 and IRAK1 in diabetic group as compared to the control group. In contrast, swimming exercise resulted in a significant decrease in expression levels of miR-146a, NF-кB and inflammatory cytokines and a significant increase in expression levels of TRAF6 and IRAK1 in the exercise-diabetic group compared to the diabetic group.


Metabolites ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 111
Author(s):  
Eunhee Cho ◽  
Da Yeon Jeong ◽  
Jae Geun Kim ◽  
Sewon Lee

Irisin is a myokine primarily secreted by skeletal muscles and is known as an exercise-induced hormone. The purpose of this study was to determine whether the PGC-1α -FNDC5 /Irisin-UCP1 expression which is an irisin-related signaling pathway, is activated by an acute swimming exercise. Fourteen to sixteen weeks old male C57BL/6J mice (n = 20) were divided into control (CON, n = 10) and swimming exercise groups (SEG, n = 10). The SEG mice performed 90 min of acute swimming exercise, while control (non-exercised) mice were exposed to shallow water (2 cm of depth) for 90 min. The mRNA and protein expression of PGC-1α, FNDC5 and browning markers including UCP1 were evaluated by quantitative real-time PCR and western blotting. Serum irisin concentration was measured by enzyme-linked immunosorbent assay. An acute swimming exercise did not lead to alterations in the mRNA and protein expression of PGC-1α in both soleus and gastrocnemius muscles, the mRNA and protein expression of UCP1 in brown adipose tissue, mRNA browning markers in visceral adipose tissue and circulating irisin when compared with the control group. On the other hand, an acute swimming exercise led to increases in the mRNA and protein expressions of FNDC5 in the soleus muscle, the protein expression of FNDC5 in the gastrocnemius muscles and the protein expression of UCP1 in subcutaneous adipose tissue.


1999 ◽  
Vol 161 (1) ◽  
pp. 153-165 ◽  
Author(s):  
DJ Hill ◽  
J Petrik ◽  
E Arany ◽  
TJ McDonald ◽  
TL Delovitch

Interleukin-1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) contribute to the initial stages of the autoimmune destruction of pancreatic beta cells. IL-1beta is released by activated macrophages resident within islets, and its cytotoxic actions include a stimulation of nitric oxide (NO) production and the initiation of apoptosis. Insulin-like growth factors (IGFs)-I and -II prevent apoptosis in non-islet tissues. This study investigated whether IGFs are cytoprotective for isolated islets of Langerhans from non-obese diabetic mice (NOD) mice exposed to cytokines. Pancreatic islets isolated from 5-6-week-old, pre-diabetic female NOD mice were cultured for 48 h before exposure to IL-1beta (1 ng/ml), TNF-alpha (5 ng/ml), IFN-gamma (5 ng/ml) or IGF-I or -II (100 ng/ml) for a further 48 h. The incidence of islet cell apoptosis was increased in the presence of each cytokine, but this was significantly reversed in the presence of IGF-I or -II (IL-1beta control 3.5+/-1.6%, IL-1beta 1 ng/ml 27.1+/-5.8%, IL-1beta+IGF-I 100 ng/ml 4.4+/-2.3%, P<0.05). The majority of apoptotic cells demonstrated immunoreactive glucose transporter 2 (GLUT-2), suggesting that they were beta cells. Islet cell viability was also assessed by trypan blue exclusion. Results suggested that apoptosis was the predominant cause of cell death following exposure to each of the cytokines. Co-incubation with either IGF-I or -II was protective against the cytotoxic effects of IL-1beta and TNF-alpha, but less so against the effect of IFN-gamma. Exposure to cytokines also reduced insulin release, and this was not reversed by incubation with IGFs. Immunohistochemistry showed that IGF-I was present in vivo in islets from pre-diabetic NOD mice which did not demonstrate insulitis, but not in islets with extensive immune infiltration. Similar results were seen for IGF-binding proteins (IGFBPs). These results suggest that IGFs protect pre-diabetic NOD mouse islets from the cytotoxic actions of IL-1beta, TNF-alpha and IFN-gamma by mechanisms which include a reduction in apoptosis.


2017 ◽  
Vol 45 (1) ◽  
pp. 5
Author(s):  
Deniz Uluisik ◽  
Ercan Keskin

Background: Coenzyme Q10 is a well-known cofactor in the mitochondrial electron transport chain required for ATP production. Coenzyme Q10 is recognized as an intracellular antioxidant that protects cell membrane phospholipids, mitochondrial membrane protein, and plasma low-density lipoprotein against oxidative damage caused by free radicals. Diabetes and its complications have been related to increased levels of free radicals and systemic proinflammatory cytokines and to an abnormal lipid profile. The aim of this study was to investigate the effects of coenzyme Q10 supplementation on some cytokine levels in streptozotocin-induced diabetic rats.Materials, Methods & Results: In this study, 38 healthy, adult male rats were used. The rats were divided into 5 groups. All animals were housed in separated cages during the four weeks. The animals in group 1 was fed standard rat pellets for 4 weeks. It was administered at 0.3 mL corn oil intraperitoneally daily for four weeks in group 2 animals. The animals in group 3 was injected intraperitoneally with 10 mg/kg CoQ10 daily for 4 weeks. Group 4 was made diabetic by subcutaneous injections of streptozotocin at dose of 40 mg/kg in 0.1 M citrate buffer (pH 4.5) single daily dose for two days and group 5 was made diabetic by subcutaneous injections of streptozotocin at dose of 40 mg/kg in 0.1 M citrate buffer (pH 4.5) single daily dose for two days and then was injected intraperitoneally with 10 mg/kg CoQ10 daily for 4 weeks. During the experiment, three animals from group 4 and one animals from group 5 were died due to streptozotocin-induced hypoglycemia. At the end of the study, blood samples were taken from all animals. In these blood samples, IL-4, IL-6, IL-10 and TNF-α plasma levels were determined with ELISA using sandwich enzyme-linked immunosorbent method via commercial kits. In this study, IL-4 level as an anti-inflammatory cytokine significantly decreased (P < 0.05) with diabetes induction compared to control group level. IL-10 level in diabetic group was statistically different (P < 0.05) from control group level. CoQ10 application to diabetic animals improved the falling in IL-10 level of diabetic group (P < 0.05). IL-6 and TNF-α levels in diabetic group significantly increased (P < 0.05) in parallel with each other compared to control group levels. The same parameters were reduced (P < 0.05) by CoQ10 application in diabetic animals.Discussion: In this study, the occurred changes in pro- and anti-inflammatory cytokines with experimentally induced diabetes are expected results and these results are consistent with some studies related diabetes. These results may be considered to hazardous effects and inflammation caused by diabetes on liver, pancreas and other tissues. CoQ10 suppressed the increments in plasma pro-inflammatory cytokine levels, whereas it restored the reducing in anti-inflammatory cytokine levels arising due to diabetes. The obtained results from this study after CoQ10 application supported similar studies used CoQ10 application against deleterious effects of diabetes in animals and humans. Therefore, it is possible to say that CoQ10 may play important role in regulation of imbalance between inflammation markers in diabetes conditions and further studies are needed to clear the beneficial effects of CoQ10 treatment on the other inflammation markers in diabetes status.


mSphere ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Alessandro Tanca ◽  
Antonio Palomba ◽  
Cristina Fraumene ◽  
Valeria Manghina ◽  
Michael Silverman ◽  
...  

ABSTRACT Increasing evidence suggests that the intestinal microbiota is involved in the pathogenesis of type 1 diabetes (T1D). Here we sought to determine which gut microbial taxa and functions vary between nonobese diabetic (NOD) mice and genetically modified NOD mice protected from T1D (Eα16/NOD) at 10 weeks of age in the time window between insulitis development and T1D onset. The gut microbiota of NOD mice were investigated by analyzing stool samples with a metaproteogenomic approach, comprising both 16S rRNA gene sequencing and microbial proteome profiling through high-resolution mass spectrometry. A depletion of Firmicutes (particularly, several members of Lachnospiraceae) in the NOD gut microbiota was observed compared to the level in the Eα16/NOD mice microbiota. Moreover, the analysis of proteins actively produced by the gut microbiota revealed different profiles between NOD and Eα16/NOD mice, with the production of butyrate biosynthesis enzymes being significantly reduced in diabetic mice. Our results support a model for gut microbiota influence on T1D development involving bacterium-produced metabolites as butyrate. IMPORTANCE Alterations of the gut microbiota early in age have been hypothesized to impact T1D autoimmune pathogenesis. In the NOD mouse model, protection from T1D has been found to operate via modulation of the composition of the intestinal microbiota during a critical early window of ontogeny, although little is known about microbiota functions related to T1D development. Here, we show which gut microbial functions are specifically associated with protection from T1D in the time window between insulitis development and T1D onset. In particular, we describe that production of butyrate biosynthesis enzymes is significantly reduced in NOD mice, supporting the hypothesis that modulating the gut microbiota butyrate production may influence T1D development.


2018 ◽  
Vol 4 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Muayad A Merza ◽  
Abdul Aziz Sulaiman Savo ◽  
Muhammad Jaafer

Diabetes can be linked with impaired host immunity that subsequently increases the rate of various infections including tuberculosis (TB), particularly in developing countries where TB is endemic. The objectives of this case control study were to determine the prevalence and the risk of LTBI among diabetic patients. It is a prospective case control study conducted in Azadi Teaching Hospital from September 2017 until May 2018. The diabetic patients included in this study were randomly selected. The diagnosis of diabetes mellitus (DM) was made according to the American Diabetes Association (ADA). Diabetes mellitus patients and the control participants were offered a voluntary tuberculin skin test (TST). The TST ≥10 mm was considered positive. The results were analyzed by entering the data in SPSS (statistical package for the social sciences, version 16; SPSS Inc., Chicago, Illinois, USA). Two hundred DM patients and 208 control individuals participated in this study. Collectively, 28 patients had positive TST results. Based on the sputum smear microscopy and CXR, none of these patients showed active TB disease. The differences between the DM patients and the control group had no statistical significance apart from previous hospitalization. The prevalence of LTBI was 23.53% in the diabetic group, whereas, it was 9.62% in the control group. The frequency of LTBI in diabetic patients was significantly higher than the control group. When the diabetic group was compared with the control group in terms of diabetic control and the duration of diabetes disease, there was a statistically significant association of diabetes duration ≥ 10 years and TST positivity. In conclusion, the previous hospitalization was a significant risk factor for diabetic patients to acquire TB bacilli. Latent TB infection was more common in diabetics than non diabetics and there was an increased likelihood of having LTBI with the duration of diabetes ≥ 10 years. To avoid the threatening of TB control program, prophylactic treatment of LTBI in diabetic patients is paramount.Asian J. Med. Biol. Res. June 2018, 4(2): 227-232


2014 ◽  
Vol 132 (2) ◽  
pp. 116-120 ◽  
Author(s):  
Luciene Setsuko Akimoto Gunther ◽  
Helen Priscila Rodrigues Martins ◽  
Fabrícia Gimenes ◽  
André Luelsdorf Pimenta de Abreu ◽  
Marcia Edilaine Lopes Consolaro ◽  
...  

CONTEXT AND OBJECTIVE: Vulvovaginal candidiasis (VVC) is caused by abnormal growth of yeast-like fungi on the female genital tract mucosa. Patients with diabetes mellitus (DM) are more susceptible to fungal infections, including those caused by species of Candida. The present study investigated the frequency of total isolation of vaginal Candida spp., and its different clinical profiles - colonization, VVC and recurrent VVC (RVVC) - in women with DM type 2, compared with non-diabetic women. The cure rate using fluconazole treatment was also evaluated. DESIGN AND SETTING: Cross-sectional study conducted in the public healthcare system of Maringá, Paraná, Brazil. METHODS: The study involved 717 women aged 17-74 years, of whom 48 (6.7%) had DM type 2 (mean age: 53.7 years), regardless of signs and symptoms of VVC. The yeasts were isolated and identified using classical phenotypic methods. RESULTS: In the non-diabetic group (controls), total vaginal yeast isolation occurred in 79 (11.8%) women, and in the diabetic group in 9 (18.8%) (P = 0.000). The diabetic group showed more symptomatic (VVC + RVVC = 66.66%) than colonized (33.33%) women, and showed significantly more colonization, VVC and RVVC than seen among the controls. The mean cure rate using fluconazole was 75.0% in the diabetic group and 86.7% in the control group (P = 0.51). CONCLUSION: We found that DM type 2 in Brazilian women was associated with yeast colonization, VVC and RVVC, and similar isolation rates for C. albicans and non-albicans species. Good cure rates were obtained using fluconazole in both groups.


2021 ◽  
Author(s):  
I.S. Al-Amri ◽  
F. Mabood ◽  
I.T. Kadim ◽  
A.Y. Alkindi ◽  
A. Al-Harrasi ◽  
...  

ABSTRACTThis study was designed to develop a rapid, sensitive, accurate, and inexpensive Fourier Transform Infrared Reflectance (FT-IR) Spectroscopy coupled with Principle Component Analysis (PCA) as a detection technique to evaluate the solubility of 11-Keto-β-Boswellic acid (KBA), from the gum resin extracted from the Omani frankincense, (Boswellia sacra) in the liver of STZ induced diabetic mice. This study also investigated the effect of KBA on the histological changes of hepatocytes of diabetic mice. Liver tissue samples from three groups of mice included normal control group, diabetic control group and diabetic group treated IP with KBA were scanned with FT-IR spectrophotometer in the reflection mode. FT-IR Spectra were collected in the wavenumber range from 400 to 4000cm-1 using ATR accessorry. The results of FT-IR Spectra were analyzed by using multivariate method Principle Component Analysis. The PCA score plot is an exploratory multivariate method indicated that there was a complete segregation among the three groups of liver samples based on change in variation of position of wavenumber in FT-IR spectra, which revealed that there is a clear effect of KBA solubility on treatments. The histological features showed an improvement in the liver tissues with normal structures of hepatocytes with exhibiting mild vacuolations in their cytoplasm. In conclusion, reflectance FT-IR spectroscopy coupled with PCA could be deployed as a new detection method for rapid, low cost and non-destructive method for evaluating of treatment effects in diseased liver tissue based on the solubility of KBA. Histological findings demonstrated the protective effective of KBA on improving the morphology of liver tissue in diabetic mice which resulted in complete recovery to the damage observed in diabetic control group.Summary StatementReflectance FT-IR spectroscopy coupled with PCA has been deployed as a new rapid, inexpensive and non-destructive detection method to examine the solubility of 11-keto-β-Boswellic acid (KBA) in streptozotocin (STZ) induced-diabetes mice liver tissue following intraperitoneal treatment. Moreover, microscopic study of liver tissue histopathology revealed that KBA has a protecting effect against STZ damage.


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