ABSTRACT
Hodgkin lymphoma is histologically characterised by the presence of Hodgkin (H) and Reed-Sternberg (RS) cells originating from germinal centre B-cells rearranged in the IgV gene. The formation of multinucleated RS cells is a product of telomere organisation in a process initiated by telomere aggregate accumulation in mononuclear H cells and may be mediated by latent membrane protein 1 (LMP-1) expression. LMP-1 is the main oncoprotein of EBV and supports several tumourigenic processes. LMP-1 may rescue proapoptotic B-cells through downregulation of B-cell receptor (BCR) components, mimicking and inducing multiple distinct B-cell signalling pathways to promote proliferation and survival, such as Janus kinase-signal transducer and activator of transcription (JAK-STAT), nuclear factor-kappa b (NF-кB), and cellular MYC (c-MYC), and inducing telomere instability mainly through Telomere repeat binding factor 2 (TRF2) downregulation to promote the formation of multinucleated RS cells. This review presents recent discoveries regarding the influence of LMP-1 on the surviving cellular signalling, genomic instability and mecanical formation of HRS cells.
Subject(s)
Herpesvirus 4, Human , Hodgkin Disease , Viral Matrix Proteins , Hodgkin Disease/virology , Hodgkin Disease/pathology , Hodgkin Disease/metabolism , Humans , Viral Matrix Proteins/metabolism , Viral Matrix Proteins/genetics , Herpesvirus 4, Human/genetics , Signal Transduction , Epstein-Barr Virus Infections/virology , Epstein-Barr Virus Infections/metabolism , Epstein-Barr Virus Infections/pathology , Genomic Instability , Reed-Sternberg Cells/metabolism , Reed-Sternberg Cells/pathology , Reed-Sternberg Cells/virologyABSTRACT
This study investigated if a prior long-term physical exercise protocol protects the substantia nigra and the striatum against oxidative stress and motor deficits in a Parkinson Disease model induced by 6-hydroxydopamine. Three animal treatment groups were included in the study: sham; 6-hydroxydopamine and 6-hydroxydopamine/exercise. Previously to the intrastriatal lesion by 6-hydroxydopamine, rats in the exercise groups performed a swimming program for 18 weeks. The rats were submitted to behavioral tests before and after intrastriatal 6-hydroxydopamine injection. The oxidative stress was analyzed by Thiobarbituric Acid Reactive Substances and Glutathione reductase activity methods. The exercise decreased lipid peroxidation and increased glutathione reductase activity in the substantia nigra. In contrast, in the striatum, exercise increased lipid peroxidation and decreased glutathione reductase activity. Exercise increased contralateral rotations and reduces immobility levels at 14 days post lesion. The exercise prior to 6-OHDA lesion had protective action only in substantia nigra against oxidative stress.
Subject(s)
Motor Skills Disorders/metabolism , Motor Skills Disorders/prevention & control , Oxidative Stress/physiology , Oxidopamine/toxicity , Parkinsonian Disorders/metabolism , Parkinsonian Disorders/prevention & control , Physical Conditioning, Animal/physiology , Animals , Male , Motor Skills Disorders/chemically induced , Oxidative Stress/drug effects , Parkinsonian Disorders/chemically induced , Physical Conditioning, Animal/methods , Random Allocation , Rats , Rats, WistarABSTRACT
PURPOSE:: To evaluate the effects of tramadol hydrochloride associated to remote ischemic perconditioning on oxidative stress. METHODS:: Twenty five male rats (Wistar) underwent right nephrectomy and were distributed into five groups: Sham group (S); Ischemia/Reperfusion group (I/R) with 30 minutes of renal ischemia; Remote ischemic perconditioning group (Per) with three cycles of 10 minutes of I/R performed during kidney ischemia; Tramadol group (T) treated with tramadol hydrochloride (40mg/kg); remote ischemic perconditioning + Tramadol group (Per+T) with both treatments. Oxidative stress was assessed after 24 hours of reperfusion. RESULTS:: Statistical differences were observed in MDA levels between I/R group with all groups (p<0.01), in addition there was difference between Tramadol with Sham, Per and Per+T groups (p<0.05), both in plasma and renal tissue. CONCLUSION:: Remote ischemic perconditioning was more effective reducing renal ischemia-reperfusion injury than administration of tramadol or association of both treatments.
Subject(s)
Ischemia/prevention & control , Ischemic Preconditioning/methods , Kidney/blood supply , Oxidative Stress/drug effects , Protective Agents/pharmacology , Reperfusion Injury/prevention & control , Tramadol/pharmacology , Animals , Combined Modality Therapy/methods , Ischemia/metabolism , Kidney/metabolism , Male , Malondialdehyde/analysis , Oxidative Stress/physiology , Random Allocation , Rats, Wistar , Reperfusion Injury/metabolism , Reproducibility of Results , Time Factors , Treatment OutcomeABSTRACT
Abstract Purpose: To evaluate the effects of tramadol hydrochloride associated to remote ischemic perconditioning on oxidative stress. Methods: Twenty five male rats (Wistar) underwent right nephrectomy and were distributed into five groups: Sham group (S); Ischemia/Reperfusion group (I/R) with 30 minutes of renal ischemia; Remote ischemic perconditioning group (Per) with three cycles of 10 minutes of I/R performed during kidney ischemia; Tramadol group (T) treated with tramadol hydrochloride (40mg/kg); remote ischemic perconditioning + Tramadol group (Per+T) with both treatments. Oxidative stress was assessed after 24 hours of reperfusion. Results: Statistical differences were observed in MDA levels between I/R group with all groups (p<0.01), in addition there was difference between Tramadol with Sham, Per and Per+T groups (p<0.05), both in plasma and renal tissue. Conclusion: Remote ischemic perconditioning was more effective reducing renal ischemia-reperfusion injury than administration of tramadol or association of both treatments.
