scholarly journals Immunohistochemical Expression of P16 Protein and TGF β1 in Mice Liver Exposed to Fumonisin B1

2020 ◽  
Vol 17 (2) ◽  
pp. 0401
Author(s):  
Sinai Mohammed et al.
Keyword(s):  
Fusarium Species ◽  
Critical Role ◽  
Fumonisin B1 ◽  
Structural Similarity ◽  
Saline Control ◽  
Control Group ◽  
Male Mice ◽  
P16 Protein ◽  
Mice Liver ◽  
Tgf Β1

Fumonisin B1 (FB1) is a mycotoxin produced in some grains (mainly corn) by Fusarium species. Due to a structural similarity between FB1 and sphinganine, sphingolipids metabolism is inhibited. Such inhibition plays a critical role in cell to cell singling and structure of lipoprotein; therefore FB1 has been suggested to have a relationship with human and animal cancer. This research is planned to study the effect of FB1 on male mice at two doses (20 and 30 µg/ ml) on the expression of TGF-β1 and p16 in liver cells. Three groups of Swiss albino male mice; each group was orally administrated with FB1 toxin as the following: normal saline (control group); 20 and 30 µg/ ml. All groups were sacrificed after two weeks of oral management. Liver samples were collected and prepared for immunohistochemistry technique (IHC) using anti-TGF-β1 and anti-p16 antibodies. The results showed that exposure to FB1 caused significant elevation of TGF-β1 in both doses (76.74 ± 2.387% and 80.62 ± 7.277%, respectively) in comparison with the control group (46.79 ± 2.404%). The level of p16 protein was decreased at 20 µg/ml (76.63 ± 2.349%) and then increased at 30 µg/ml (81.25 ± 6.263%) but the expression was lower than that of control (90.00 ± 0.805%). In conclusion, FB1 has a significant effect on TGF-β1 and p16 protein expression at both doses (20 and 30 µg/ml), and therefore, its role in cancer development is suggested.

scholarly journals FumDSB Can Reduce the Toxic Effects of Fumonisin B1 by Regulating Several Brain-Gut Peptides in Both the Hypothalamus and Jejunum of Growing Pigs

Toxins ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 874
Author(s):  
Quancheng Liu ◽  
Fuchang Li ◽  
Libo Huang ◽  
Wenjie Chen ◽  
Zhongyuan Li ◽  
...  
Keyword(s):  
Fusarium Species ◽  
Animal Health ◽  
Fumonisin B1 ◽  
Basal Diet ◽  
Growing Pigs ◽  
Control Group ◽  
Gut Peptides ◽  
Potential Threat ◽  
Animal Trials ◽  
Food Borne

Fumonisin B1 (FB1) is the most common food-borne mycotoxin produced by the Fusarium species, posing a potential threat to human and animal health. Pigs are more sensitive to FB1 ingested from feed compared to other farmed livestock. Enzymatic degradation is an ideal detoxification method that has attracted much attention. This study aimed to explore the functional characteristics of the carboxylesterase FumDSB in growing pigs from the perspective of brain–gut regulation. A total of 24 growing pigs were divided into three groups. The control group was fed a basal diet, the FB1 group was supplemented with FB1 at 5 mg/kg feed, and the FumDSB group received added FumDSB based on the diet of the FB1 group. After 35 days of animal trials, samples from the hypothalamus and jejunum were analyzed through HE staining, qRT-PCR and immunohistochemistry. The results demonstrated that the ingestion of FB1 can reduce the feed intake and weight gain of growing pigs, indicating that several appetite-related brain-gut peptides (including NPY, PYY, ghrelin and obestatin, etc.) play important roles in the anorexia response induced by FB1. After adding FumDSB as detoxifying enzymes, however, the anorexia effects of FB1 were alleviated, and the expression and distribution of the corresponding brain-gut peptides exhibited a certain degree of regulation. In conclusion, the addition of FumDSB can reduce the anorexia effects of FB1 by regulating several brain-gut peptides in both the hypothalamus and the jejunum of growing pigs.

scholarly journals Cisplatin-induced neurotoxicity in cerebellar cortex of male mice involves oxidative stress and histopathology

2021 ◽  
Vol 82 (1) ◽  
Author(s):  
Azza Attia ◽  
Cecil Matta ◽  
Reda ElMazoudy ◽  
Hanan Khalifa
Keyword(s):  
Oxidative Stress ◽  
Cerebellar Cortex ◽  
Molecular Layer ◽  
Nerve Fibers ◽  
The Body ◽  
Saline Control ◽  
Control Group ◽  
Cortical Region ◽  
Male Mice ◽  
Stress Dependent

Abstract Background Despite evidence of neurotoxicity, cisplatin is still considered the most potent drug prescribed in human chemotherapy for a broad spectrum of malignancies. The objective was to evaluate the cerebellar cortex damage including oxidative stress biomarkers and histopathology aspects in male mice. One saline control group and two cisplatin groups were intraperitoneally injected with 0, 5, and 10 mg/kg body weight (bw) cisplatin, twice per week for four successive weeks, respectively. Results Cisplatin decreased the body weights of treated mice. Serum levels of superoxide dismutase and glutathione peroxidase were significantly reduced in the 5 and 10 mg/kg dose, twice weekly for 4 weeks treatment; in contrast, there was a significant increase of lipid peroxidation. 5 and 10 mg/kg bw of cisplatin caused histopathological damage in the cerebellum tissue characterized by disruption, disorganization, and degeneration with dense pyknotic nuclei of the granular cells. Ultrastructurally, in the cortical region of the cerebellum, the Purkinje cells showed irregular pyknotic nuclei with indistinct nucleoli, cytoplasmic vacuolation, marked indentation of the nuclear membrane, dilatation of the endoplasmic reticulum, and breakdown and disappearance of mitochondrial cristae. Moreover, the molecular layer showed cellular necrosis and an increased number of lysosomal particles. The myelinated nerve fibers showed degenerative areas distinct by splitting, disruption, and loss of the lamellar pattern of the myelin sheath. Conclusion These findings provide a confirmed foresight that the in vivo potential treatment of mice with cisplatin induces cerebellum deficits and impairment in neuronal histology. The identified mechanism which evokes neurotoxicity is oxidative stress-dependent status. This mechanism is pharmacologically boosted by great production of free radical reactive oxygen species.

scholarly journals Small Interference RNA Targeting TLR4 Gene Effectively Attenuates Pulmonary Inflammation in a Rat Model

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Feixiang Wu ◽  
Yantao Liu ◽  
Xin Lv ◽  
Xuerong Miao ◽  
Yuming Sun ◽  
...  
Keyword(s):  
Lung Injury ◽  
Critical Role ◽  
Saline Control ◽  
Control Group ◽  
Tlr4 Expression ◽  
Small Interference Rna ◽  
Tlr4 Gene ◽  
Interference Rna

Objective. The present study was to investigate the feasibility of adenovirus-mediated small interference RNA (siRNA) targeting Toll-like receptor 4 (TLR4) gene in ameliorating lipopolysaccharide- (LPS-) induced acute lung injury (ALI).Methods.In vitro, alveolar macrophages (AMs) were treated with Ad-siTLR4 and Ad-EFGP, respectively, for 12 h, 24 h, and 48 h, and then with LPS (100 ng/mL) for 2 h, and the function and expression of TLR4 were evaluated.In vivo, rats received intratracheal injection of 300 μL of normal saline (control group), 300 μL of Ad-EGFP (Ad-EGFP group), or 300 μL of Ad-siTLR4 (Ad-siTLR4 group) and then were intravenously treated with LPS (50 mg/kg) to induce ALI.Results. Ad-siTLR4 treatment significantly reduced TLR4 expression and production of proinflammatory cytokines following LPS treatment bothin vitroandin vivo. Significant alleviation of tissue edema, microvascular protein leakage, and neutrophil infiltration was observed in the AdsiTLR4-treated animals.Conclusion. TLR4 plays a critical role in LPS-induced ALI, and transfection of Ad-siTLR4 can effectively downregulate TLR4 expressionin vitroandin vivo, accompanied by alleviation of LPS-induced lung injury. These findings suggest that TLR4 may serve as a potential target in the treatment of ALI and RNA interfering targeting TLR4 expression represents a therapeutic strategy.

Effect of Oral Honey Administration on Sleep-Deprived Male Mice

2020 ◽  
Vol 1 (3) ◽  
pp. 41-53
Author(s):  
E.I Akinyemi ◽  
◽  
M.A, Akanmu ◽  
K.M. Adeoluwa ◽  
◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Critical Role ◽  
Young Male ◽  
Inhibitory Effect ◽  
Control Group ◽  
Male Mice ◽  
Optimal Health ◽  
Biologic Process ◽  
Hole Board ◽  
Hole Board Test

Background: Sleep is a biologic process that is essential for life and optimal health. Sleep plays a critical role in brain function and systemic physiology. The deleterious health consequences of sleep deprivation are associated with risks for a wide variety of medical conditions. Honey’s potential role in restorative sleep may have implications in improving long term health. Objective: To determine the effect of honey on sleep deprivation in male mice. Method: The study was carried out using four (4) groups of young male mice (N=5-6 per group) deprived of sleep for a period of 6 hours. Bee honey was administered orally at three dose levels; 10 %, 20 % and 40 % V/v respectively to three groups while the control group was administered normal saline (vehicle). Novelty-Induced Behaviour (NIB), Elevated plus-maze (EPM), Hole board and Y-maze models were used to evaluate the effects of honey on the mice. Results: In the NIB model, a significant (p<0.05) decrease in locomotion was observed dose-dependently. The same observation was recorded for rearing behaviour while a biphasic effect was observed in grooming behaviour. The results obtained in the other models showed that locomotor activity was significantly decreased suggesting that honey has central inhibitory effect. In the hole board test and EPM, there were significantly (p<0.05) decreased activity of the mice due to the administration of honey. Conclusion: This study demonstrates that honey exerts dose-dependent central inhibitory effects in sleep-deprived male mice therefore suggesting possible amelioration of sleep deprivation effects.

A review of the toxic effects and mechanisms of action of fumonisin B1

2008 ◽  
Vol 27 (11) ◽  
pp. 799-809 ◽  
Author(s):  
H Stockmann-Juvala ◽  
K Savolainen
Keyword(s):  
Fusarium Species ◽  
Fusarium Verticillioides ◽  
Fumonisin B1 ◽  
Structural Similarity ◽  
Mechanisms Of Action ◽  
Agricultural Products ◽  
Ceramide Synthase ◽  
Fusarium Mycotoxins ◽  
Cellular Mechanisms ◽  
Toxic Potential

Fumonisin B1 (FB1) is a mycotoxin produced by the fungus Fusarium verticillioides, which commonly infects corn and other agricultural products. Fusarium species can also be found in moisture-damaged buildings, and, therefore, exposure of humans to Fusarium mycotoxins including FB1 may take place. FB1 bears a clear structural similarity to the cellular sphingolipids, and this similarity has been shown to disturb the metabolism of sphingolipids by inhibiting the enzyme ceramide synthase leading to accumulation of sphinganine in cells and tissues. FB1 is neurotoxic, hepatotoxic, and nephrotoxic in animals, and it has been classified as a possible carcinogen to humans. The cellular mechanisms behind FB1-induced toxicity include the induction of oxidative stress, apoptosis, and cytotoxicity, as well as alterations in cytokine expression. The effects of FB1 on different parameters vary markedly depending on what types of cells are studied or what species they originate from. These aspects are important to consider when evaluating the toxic potential of FB1.

scholarly journals Inhibition of TRPC6 Signal Pathway Alleviates Podocyte Injury Induced by TGF-β1

2017 ◽  
Vol 41 (1) ◽  
pp. 163-172 ◽  
Author(s):  
Haiting Huang ◽  
Yanwu You ◽  
Xu Lin ◽  
Chunrong Tang ◽  
Xiangjun Gu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Critical Role ◽  
Signal Pathway ◽  
Control Group ◽  
Caspase 9 ◽  
Podocyte Injury ◽  
Apoptosis Rate ◽  
Tgf Β1

Background/Aims: Transforming growth factor beta 1 (TGF-β1) plays a critical role in the pathogenesis of glomerulosclerosis. The purpose of this study was to examine the effects of inhibition of transient receptor potential cation channel C6 (TRPC6) on podocyte injury induced by TGF-β1 via nephrin and desmin mechanisms. Methods: A rat model of nephropathy was first induced by intravenous injections of adriamycin to determine TRPC6 signal pathway engaged in glomerulosclerosis in vivo. Conditionally immortalized podocytes were cultured in vitro and they were divided into four groups: control; TGF-β1 treatment; TGF-β1 with TRPC6 knockdown and TGF-β1 without TRPC6 knockdown. Real time RT-PCR and Western blot analysis were employed to determine the mRNA and protein of expression of nephrin, desmin and caspase-9, respectively. Flow cytometry was used to examine the apoptotic rate of podocytes and DAPI fluorescent staining was used to determine apoptotic morphology. Results: In vivo experiment, adriamycin significantly upregulated the protein expression of TGF-β1, TRPC6, desmin and caspase-9, and decreased nephrin. Consistent with the latter results, in vitro experiment mRNA and protein expression of desmin and caspase-9 was increased in cultured TGF-β1-treated podocytes, whereas nephrin was declined as compared with the control group. Importantly, TRPC6 knockdown significantly attenuated the upregulated desmin and caspase-9, and alleviated impairment of nephrin induced by TGF-β1. Moreover, typical morphologic features were presented in apoptotic podocytes. The number of apoptotic podocytes was increased after exposure to TGF-β1 and this was alleviated after TRPC6 knockdown. TRPC6 knockdown also decreased an apoptosis rate of TGF-β1-treated podocytes. Note that negative TRPC6 transfection control failed to alter an increase of the apoptosis rate in TGF-β1-treated podocytes. Conclusions: TGF-β1 induced by glomerulosclerosis impairs the protein expression of nephrin and amplifies the protein expression of desmin and caspase -9 via TRPC6 signal pathway. Inhibition of TRPC6 alleviates these changes in podocytes-treated with TGF-β1 and attenuated apoptosis of podocytes. Our data suggest that TRPC6 signal plays an important role in mediating TGF-β1-induced podocyte injury via nephrin, desmin and caspase-9. Results of the current study also indicate that blocking TRPC6 signal pathway has a protective effect on podocyte injury. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of podocyte injury observed in glomerulosclerosis.

Salivary mir-27b Expression in Oral Lichen Planus Patients: A Series of Cases and a Narrative Review of Literature

2020 ◽  
Vol 19 (31) ◽  
pp. 2816-2823 ◽  
Author(s):  
Dario Di Stasio ◽  
Laura Mosca ◽  
Alberta Lucchese ◽  
Donatella Delle Cave ◽  
Hiromichi Kawasaki ◽  
...  
Keyword(s):  
Lichen Planus ◽  
Oral Lichen Planus ◽  
Inflammatory Diseases ◽  
Biological Fluids ◽  
Critical Role ◽  
Invasive Procedure ◽  
Control Group ◽  
Study Group ◽  
Immune Functions ◽  
Oral Lichen

Background: microRNAs play a critical role in auto-immunity, cell proliferation, differentiation and cell death. miRNAs are present in all biological fluids, and their expression is essential in maintaining regular immune functions and preventing autoimmunity, whereas miRNA dysregulation may be associated with the pathogenesis of autoimmune and inflammatory diseases. Oral lichen planus (OLP) is an inflammatory disease mediated by cytotoxic T cells attack against epithelial cells. The present study aims to perform a specific microRNA expression profile through the analysis of saliva in this disease. Methods: The study group was formed by five patients (mean age 62.8±1.98 years; 3 females/2 males) affected by oral lichen planus and control group by five healthy subjects (mean age 59.8 years±2.3; 3 females/ 2 males); using a low-density microarray analysis, we recorded a total of 98 differentially expressed miRNAs in the saliva of patients with oral lichen planus compared to the control group. The validation was performed for miR-27b with qRT-PCR in all saliva samples of oral lichen planus group. Results: 89 miRNAs were up-regulated and nine down-regulated. In details, levels of miR-21, miR- 125b, miR-203 and miR15b were increased (p<0.001) in study group while levels of miR-27b were about 3.0-fold decreased compared to controls (p<0.001) of miR-27b expression in OLP saliva. QRTPCR validation confirmed the down regulation of miR-27b in all saliva samples. Conclusions: Collecting saliva samples is a non-invasive procedure and is well accepted by all patients. microRNAs can be readily isolated and identified and can represent useful biomarkers of OLP.

Efek Ekstrak Etanol Kulit Petai (Parkia speciosa Hassk) Terhadap Penurunan Kadar Glukosa Darah Mencit Jantan

2018 ◽  
Vol 3 (1) ◽  
pp. 1
Author(s):  
Verawaty Verawaty ◽  
Dhea Claudia Novel
Keyword(s):  
Blood Glucose ◽  
Ethanol Extract ◽  
Negative Control Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Male Mice ◽  
Glucose Levels ◽  
The Third ◽  
Blood Glucose Levels

<p>Penelitian ini bertujuan untuk melihat pengaruh pemberian ekstrak etanol kulit petai (Parkia speciosa Hassk) terhadap penurunan kadar glukosa darah mencit jantan yang diinduksi aloksan. Hewan percobaan dibagi atas 5 kelompok diantaranya kelompok kontrol negatif, kelompok kontrol positif,dosis I (280 mg/kgBB mencit), dosis II (560 mg/kg BB mencit), dosis III (840 mg/kg BB mencit). Penelitian dilakukan selama 21 hari. Persentase penurunan kadar glukosa darah mencit jantan setelah diberikan ekstrak etanol kulit petai pada hari ke-21 adalah dosis I (77,52 %) lebih besar dibandingkan dengan dosis II (69,5 %) dan dosis III (73,37 %). Data yang diperoleh dianalisis dengan uji Two Way Anova dengan program SPSS 17. Hasil penelitian ini menunjukkan bahwa pemberian ekstrak etanol kulit petai untuk tiga variasi dosis menyatakan perbedaan yang bermakna secara statistik terhadap penurunan kadar glukosa darah mencit jantan.</p><p><em>Petai (Parkia speciosa Hassk) has a compound β-sitosterol and stigmasterol that have efficacy to decreased blood glucose levels. This study aimed to determine the effect of ethanol extract of petai peel for decrease blood glucose levels of male mice induced by alloxan. Experimental animals were divided into 5 groups including negative control group, positive control group, the first dose (280 mg/kg in mice), the second dose (560 mg/kg in mice), the third dose (840 mg/kg in mice). The study was conducted for 21 days. After 21 days, the result found that the percentage of blood glucose levels after the male mice given the ethanol extract of petai peel was, the first dose (77.52%) biger than the second dose (69.5%) and the third dose (73.37%). The data obtained were analyzed by Two Way ANOVA using SPSS 17. The results showed that have signicantly difference between three dose variation of ethanol extract of petai peel in blood glucose levels.</em></p>

Comparative effects of Orchis anatolica vs. the red Korean Panax ginseng treatments on testicular structure and function of adult male mice

2015 ◽  
Vol 12 (1) ◽  
Author(s):  
Nabil A. Khouri ◽  
Haytham M. Daradka ◽  
Mohammed Z. Allouh ◽  
Ahmad S. Alkofahi
Keyword(s):  
Panax Ginseng ◽  
Male Fertility ◽  
Virgin Female ◽  
Reproductive Organs ◽  
Serum Markers ◽  
Structure And Function ◽  
Control Group ◽  
Male Mice ◽  
Fertility Potential ◽  
And Function

Abstract: The effects of: Both plants were administered orally to two separate mice groups at a dose of 800 mg/kg/day for 35 days and compared with control group. After treatment, 5 mice of each group were sacrificed and total mice weights, reproductive organs’ weights, spermatogenesis, and androgenic serum markers were investigated. The remaining mice from all groups were allowed to mate with virgin female mice to explore male fertility potential.: Results indicated that body and organs’ weights were increased significantly in mice treated with: We can conclude that

scholarly journals Exogenous Transforming Growth Factor-β in Brain-Induced Symptoms of Central Fatigue and Suppressed Dopamine Production in Mice

2021 ◽  
Vol 22 (5) ◽  
pp. 2580
Author(s):  
Won Kil Lee ◽  
Yeongyeong Kim ◽  
Heejin Jang ◽  
Joo Hye Sim ◽  
Hye Jin Choi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Neuroblastoma Cell ◽  
Critical Role ◽  
Central Fatigue ◽  
Chronic Fatigue ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Intracranial Injection ◽  
Tgf Β1

Myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) is one of the most refractory diseases in humans and is characterized by severe central fatigue accompanied with various symptoms that affect daily life, such as impaired memory, depression, and somatic pain. However, the etiology and pathophysiological mechanisms of CFS remain unknown. To investigate the pathophysiological role of transforming growth factor (TGF)-β1, we injected a cytokine into the lateral ventricle of a C57BL/6 mouse. The intracranial injection of TGF-β1 increased the immobility duration in a forced swimming test (FST) and time spent at the closed arm in elevated plus maze (EPM) analysis. The mice injected with TGF-β1 into their brain showed increased sensitivity to pain in a von Frey test, and had a decreased retention time on rotarod and latency time in a bright box in a passive avoidance test. In addition, the serum levels of muscle fatigue biomarkers, lactate dehydrogenase (LDH) and creatine kinase (CK), were significantly increased after administration of TGF-β1. Intracranial injection of TGF-β1 significantly reduced the production of tyrosine hydroxylase (TH) in the ventral tegmental area, accompanied by a decreased level of dopamine in the striatum. The suppression of TH expression by TGF-β1 was confirmed in the human neuroblastoma cell line, SH-SY5Y. These results, which show that TGF-β1 induced fatigue-like behaviors by suppressing dopamine production, suggest that TGF-β1 plays a critical role in the development of central fatigue and is, therefore, a potential therapeutic target of the disease.

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