The role of autophagy-related gene 9B in lichen planus

Background: Lichen planus (LP) is an idiopathic, chronic, relapsing, inflammatory, autoimmune dermatological disease. The etiopathogenesis of LP is still unclear. Autophagy is a strictly regulated lysosomal degradation pathway that is crucial for maintaining intracellular homeostasis and normal development. The dysregulation of autophagy-associated genes was recognized to increase the susceptibility to multiple diseases, including inflammation, autoimmune disorders and cancer. Aims: Our study aimed to detect the expression of autophagy-related gene 9 b (ATG9B) in LP patients compared to normal control persons to investigate the possible role of autophagy in pathogenesis of this disease. Methods: This case–control study included 30 LP patients and 30 age-, gender-matched healthy controls. Four millimeters punch skin biopsies were obtained from LP lesions and from the controls and they were kept in lysis solution for the stability of the studied parameters and were kept frozen at –80°C till analysis of ATG9B using real-time polymerase chain reaction. Results: The level of ATG9B in lesional skin of LP was significantly decreased compared to normal control persons (P < 0.01); also, there was a non-significant relation between ATG9B level and age, sex, duration and family history among LP patients. Limitations: Limited number of patients included in our study (30 patients). Conclusion: Autophagy may play a role in the pathogenesis of cutaneous LP.

Evaluation of Glucosamine Effect Against Heart and Brain Damage Induced by Y-radiation or Aluminium Chloride in Female Rats

Abstract Glucosamine is known as anti-inflammatory, antioxidant and as neuroprotective as well as using to treat many of diseases. This work aimed to investigate the remedial effect of glucosamine (20mg/kg b.wt) against the damage induced by a single dose of γ-radiation (8Gy) or aluminium chloride (AlCl3) (100mg/kg b.wt) in the heart and brain tissues of female rats. Serum aspartate aminotransferase (AST), cholesterol, triglycerides (TGs), LDH and creatine kinase (CPK) were measured. Moreover, gene expression of amyloid protein precursor (APP) and seladin-1 were estimated in the brain tissue. Also, acetylcholinesterase activity (AChE) and p-tau protein expression were estimated in brain homogenate. Metallothioneine (MT) was estimated in the heart and brain tissues. Heart and brain histopathological examination was performed. Irradiation significantly decreased serum AST, CPK and LDH, as well as MT levels in heart and brain tissues. Also, gene expression of seladin-1 decreased. On the other hand, irradiation significantly increased serum TGs level and brain AchE activity, tau protein, and β-amyloid percursor (APP). AlCl3 administration (21 days) induced disturbance in most of the estimated parameters, especially AST, TGs, and MT. Glucosamine treatment with irradiation or AlCl3 improved most of the measured parameters. In addition, histopathological examination confirmed the biochemical results. In conclusion: Glucosamine could be used to improve the heart and brain damages induced by γ-radiation exposure or AlCl3.

Bone Marrow Mesenchymal Stem Cells Regulate Coagulation and Inflammation Together in Methotrexate Induced Lung Injury Rat Model

Abstract Clinical research has shed the light on the relation between coagulation and inflammation. Coagulation cascade is activated in lung injury resulting in thrombotic and fibrotic lesions. Such a cascade is initiated by inflammation, then the two systems intense each other. New therapies that modulate coagulation and inflammation will be more successful than therapies targeting only one of them. Mesenchymal stem cells showed anti-inflammatory functions in animal models. The role of mesenchymal stem cells in methotrexate induced lung injury model was evaluated, but no studies scoped on the role of stem cells in coagulation associated with inflammation in such models. This study focuses on the therapeutic role of mesenchymal stem cells against the development of clotting in methotrexate induced lung injury rat model. Results showed that mesenchymal stem cells treatment for 4 weeks caused a decrease in lung activated coagulation factors; protease activated receptor-1, fibrinogen, plasminogen activator inhibitor-1 and platelet count with a decrease in inflammatory factors; tumor necrosis factor-α, interferon- γ, interleukin-8, monocyte chemoattractant protein-1 and total leukocyte count. Thus, mesenchymal stem cells have anti-inflammatory potency against clotting risk in methotrexate induced lung injury model. This opens the outlook for stem cells as a new therapy that moderates coagulation associated with inflammation.

Role of Vitamin D and Metformine on Pancreatic Tissue in an Experimental Model of Type II Diabetes Mellitus

Background: The study was done to evaluate the role of Vitamin D (Vit D) in an experimental model of type II DM and compare its effects with oral hypoglycemic drugs (Metformine). Methods: 30 male rats were divided; control group, Diabetic group via administration of high fat diet then injection of streptozotocin . Diabetic rats were then divided into Diabetic group, Diabetic + Metformine group(n=6), Diabetic +Vit D (n=6), Diabetic + Metformine +Vit D (n=6). Fasting glucose, insulin, HOMA IR, Cholesterol, Triglycerides, C-Reactive protein (CRP), Glucagon like peptide (GLP1), Cyclooxygenase 2 (COX2) and Superoxide dismutase (SOD) were measured, Real time PCR for pancreatic expression levels of Caspase 3, IKKβ and Western plot of Pancreatic protein kinase beta (Akt) and INGAP (islet neogensis associated protein), and histopathological, immunohistochemical for pancreatic tissue. Results: Increased glucose, fasting insulin, HOMA IR , cholesterol, triglycerides, CRP, COX2 and expression of levels of Caspase 3 and  IK Kinase B and Akt in diabetic group in comparison to control. On the other hand, significant decreased levels of GLP1, SOD and INGAP in diabetic in comparison to control. On treatment with metformine or Vitamin D improved all parameters. In combined metformine and vitamin D therapy there was much improvement with no significant change from control. Conclusions: Vitamin D and metformine improved inflammatory, oxidative stress, apoptotic conditions in an experimental model of type II DM and combined therapy causes more improvement, so it is better to give combined therapy.