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1.
Rev Int Androl ; 22(1): 44-52, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38735877

ABSTRACT

Whether chronic inflammation in the genital tract induced by obesity shares in spermatogenic dysfunction is not clearly known. We aimed to study the effect of high fat diet (HFD) on spermatogenesis, seminal oxidative stress (malondialdehyde (MDA)) and inflammatory markers (high mobility group box 1 (HMGB1), nucleotide-binding oligomerization domain, leucine rich repeat and pyrin-3 domain containing (NLRP3)) in the rat testes and the role of zinc on testicular dysfunction and chronic inflammation in high fat diet (HFD) fed rat testes. This parallel group comparative experimental study included 36 male wistar rats divided into 3 groups: group A (fed on normal control diet); group B (fed on high fat diet (HFD) only); and group C (fed on HFD with zinc supplementation 3.2 mg/kg/day orally). At the end of the 12th week, sperm count, viability and motility were assessed by computer-assisted seemen analysis (CASA), seminal malondialdehyde measured by calorimetry and histopathological examination of testicular sections was done. Immunohistochemical staining was done for HMGB1 and NLRP3 evaluation. Sperm count was lowest in group B. Groups A and C showed statistically significant higher mean sperm vitality, total and progressive motility scores (p < 0.001), while no difference was found between the groups A and C (p > 0.05). Seminal malondialdehyde level was significantly highest in group B. Tubular diameter, epithelial height and Johnsen score were significantly lowest in group B. Significantly higher HMGB1 and NLRP3 levels were demonstrated in group B (p < 0.001). Obesity is associated with testicular dysfunction, testicular oxidative stress and increased testicular HMGB1 and NLRP3. We suggest a beneficial effect of zinc on testicular function in HFD-rats.


Subject(s)
Diet, High-Fat , HMGB1 Protein , Inflammasomes , NLR Family, Pyrin Domain-Containing 3 Protein , Oxidative Stress , Spermatogenesis , Testis , Zinc , Animals , Male , Rats , Diet, High-Fat/adverse effects , HMGB1 Protein/drug effects , HMGB1 Protein/metabolism , Inflammasomes/drug effects , Inflammasomes/metabolism , Inflammation/etiology , Inflammation/metabolism , Malondialdehyde/metabolism , Malondialdehyde/analysis , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Obesity/metabolism , Oxidative Stress/drug effects , Rats, Wistar , Sperm Count , Sperm Motility/drug effects , Spermatogenesis/drug effects , Spermatozoa/drug effects , Testis/drug effects , Testis/metabolism , Zinc/pharmacology
2.
Fundam Clin Pharmacol ; 38(4): 718-729, 2024 Aug.
Article in English | MEDLINE | ID: mdl-38279557

ABSTRACT

BACKGROUND: Spermidine is a natural biologically active substance that has widespread influences on the body. OBJECTIVE: This study aims to enhance our understanding of the potential effect of spermidine on long non-coding RNA MALAT1 and explore the underlying mechanism in the rotenone-induced rat model of Parkinson's disease. METHODS: Rats were sacrificed after locomotor behavioral testing. Striatal tissues were used to assess the expression of MALAT1, oxidative stress markers, and autophagy markers. RESULTS: Our study found that treatment with spermidine for 2 weeks during the induction of the model significantly improved behavioral assessment, dopamine levels, and attenuated the histopathological changes that occurred in PD in comparison to the non-treated group. CONCLUSION: Our preliminary study supports the protective effect of spermidine on the activation of autophagy and its antioxidant properties. Part of the antioxidant activity is due to the inhibition of MALAT1. However, MALAT1 does not correlate with the spermidine-induced autophagy pathway.


Subject(s)
Autophagy , Disease Models, Animal , Oxidative Stress , RNA, Long Noncoding , Rotenone , Spermidine , Animals , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Rotenone/toxicity , Spermidine/pharmacology , Rats , Male , Autophagy/drug effects , Oxidative Stress/drug effects , Antioxidants/pharmacology , Parkinson Disease/drug therapy , Dopamine/metabolism , Rats, Wistar
3.
Life Sci ; 309: 120988, 2022 Nov 15.
Article in English | MEDLINE | ID: mdl-36155181

ABSTRACT

AIMS: Pulmonary fibrosis (PF) is considered as an end stage for many lung diseases. Mesenchymal stem cells (MSC) as regenerative therapy have become a remarkably valuable therapeutic strategy in different diseases. Hydrogen sulfide has been recently introduced into the medical field for its antifibrotic properties in addition to enhancement of MSC stemness and function. The aim of the present study was to investigate the ability of BM-MSC in combination with NaHS to attenuate Bleomycin induced pulmonary fibrosis was studied in rats. A special emphasis was given to miR-21 and GAS5 as important players in the development of PF. MAIN METHODS: PF was induced in 32 Wistar male rats by single endotracheal injection of bleomycin, those were randomly divided into four groups (8 rats each): (untreated PF group) - (PF + MSC) treated group- (PF + NaHS treated group) - PF + combined (NAHS + MSC) treated group. KEY FINDINGS: Induction of PF was associated with increased miR-21 and decreased lncRNA-GAS5 expression. Treatment with either NaHS or BM-MSC leads to an inhibitory effect on pulmonary fibrosis as evidenced by improvement of histopathological studies, pulmonary function tests, reduction of inflammatory and fibrotic markers like Hydroxyproline, TNF α, TGF-ß and caspase -3 together with downregulation miR-21 and increase lncRNA-GAS5 expression. SIGNIFICANCE: The current work revealed the inhibitory effect of combined NaHS and BM-MSC on pulmonary fibrosis with concomitant modulation of miR-21 and lncRNA-GAS5 expression.


Subject(s)
Hydrogen Sulfide , Mesenchymal Stem Cells , MicroRNAs , Pulmonary Fibrosis , RNA, Long Noncoding , Animals , Male , Rats , Bleomycin , Bone Marrow/metabolism , Caspases/metabolism , Hydrogen Sulfide/metabolism , Hydroxyproline/metabolism , MicroRNAs/genetics , MicroRNAs/metabolism , Pulmonary Fibrosis/chemically induced , Pulmonary Fibrosis/genetics , Pulmonary Fibrosis/therapy , Rats, Wistar , RNA, Long Noncoding/metabolism , Transforming Growth Factor beta/metabolism , Tumor Necrosis Factor-alpha/metabolism
4.
Arch Physiol Biochem ; 126(4): 326-334, 2020 Oct.
Article in English | MEDLINE | ID: mdl-30449203

ABSTRACT

Context: Alzheimer's disease is strongly associated with brain insulin signalling.Objective: Investigating the effect of amylin as a novel treatment in streptozotocin (STZ) rat model of AD.Materials and methods: Alzheimer's disease (AD) was induced in albino rats by intracerebroventricular injection of STZ (3 mg/kg). Rats received either amylin analogue (Pramlintide 200 µg/kg/day) or Metformin (30 mg/kg/day) for 5 weeks.Results: Both Pramlintide and Metformin improve learning and memory through enhancing insulin signalling (p-IR and p-PI3K) which lead to lowering level of CSF glucose, phosphorylated tau proteins, and amyloid-ß peptide (Aß) in hippocampus.Conclusions: Insulin sensitisers as Metformin and Pramlintide can improve learning and memory and decrease the pathological changes in STZ induced rat model of AD. However, Pramlintide is superior to Metformin in some memory tests which related to its action as an amylin analogue. Amylin improves learning and memory through an independent effect other than insulin sensitisation.


Subject(s)
Alzheimer Disease/metabolism , Insulin Resistance , Islet Amyloid Polypeptide/pharmacology , Memory/drug effects , Alzheimer Disease/physiopathology , Animals , Avoidance Learning/drug effects , Cognition/drug effects , Disease Models, Animal , Gene Expression Regulation, Enzymologic/drug effects , Glucose/cerebrospinal fluid , Hippocampus/drug effects , Hippocampus/metabolism , Islet Amyloid Polypeptide/blood , Male , Maze Learning/drug effects , Phosphatidylinositol 3-Kinase/metabolism , Phosphorylation/drug effects , Rats , Receptor, Insulin/metabolism
5.
Can J Physiol Pharmacol ; 97(7): 638-646, 2019 Jul.
Article in English | MEDLINE | ID: mdl-30840489

ABSTRACT

Myocardial infarction is a major cause of cardiac dysfunction. All components of the cardiac renin-angiotensin system (RAS) are upregulated in myocardial infarction. Angiotensin-converting enzyme (ACE) and ACE2 are key enzymes involved in synthesis of components of RAS and provide a counter-regulatory mechanism within RAS. We compared the cardioprotective effect of the ACE2 activator diminazene aceturate (DIZE) versus the ACE inhibitor enalapril on post acute myocardial infarction (AMI) ventricular dysfunction in rats. Adult male rats received subcutaneous injections of either saline (control) or isoproterenol (85 mg/kg) to induce AMI. Rats with AMI confirmed biochemically and by ECG, were either left untreated (AMI) or administered DIZE (AMI + DIZE) or enalapril (AMI + enalapril) daily for 4 weeks. DIZE caused a significant activation of cardiac ACE2 compared with enalapril. DIZE caused a significantly greater enhancement of cardiac hemodynamics. DIZE also caused greater reductions in heart-type fatty acid binding protein (H-FABP), ß-myosin heavy chain (ß-MYH), and in heart mass to total body mass ratio. These results indicated that activation of cardiac ACE2 by DIZE enhanced the protective axis of RAS and improved myocardial function following AMI, whereas enalapril was not sufficient to restore all cardiac parameters back to normal.


Subject(s)
Angiotensin-Converting Enzyme Inhibitors/pharmacology , Cardiotonic Agents/pharmacology , Diminazene/analogs & derivatives , Enalapril/pharmacology , Myocardial Infarction/physiopathology , Peptidyl-Dipeptidase A/metabolism , Acute Disease , Angiotensin-Converting Enzyme 2 , Animals , Diminazene/pharmacology , Enzyme Activation/drug effects , Heart Ventricles/drug effects , Heart Ventricles/physiopathology , Hypertrophy, Right Ventricular/complications , Male , Myocardial Infarction/complications , Rats , Rats, Wistar
6.
Hypertens Pregnancy ; 38(3): 149-156, 2019 Aug.
Article in English | MEDLINE | ID: mdl-30922121

ABSTRACT

Background: Preeclampsia (PE) is a disorder of pregnancy associated with vitamin D (VD) deficiency. Chemerin is an adipokine significantly increased in preeclampsia and is regulated by VD. Objectives: To determine whether VD supplementation would protect against development of PE through Chemerin reduction Methods: PE was induced in albino rats by injection of 12.5 mg of deoxycorticosterone (DOCA).   Rats were randomly divided into normal pregnant, PE group, VD supplemented PE group. Results: VD supplementation decreased systolic blood pressure, proteinuria and decreased serum Chemerin level. Conclusion: VD treatment reduced Chemerin level, and blood pressure in DOCA rat model of PE.


Subject(s)
Blood Pressure/drug effects , Chemokines/blood , Pre-Eclampsia/drug therapy , Proteinuria/drug therapy , Vitamin D/therapeutic use , Animals , Dietary Supplements , Disease Models, Animal , Female , Pre-Eclampsia/blood , Pregnancy , Proteinuria/blood , Rats , Vitamin D/administration & dosage
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