Protective action of OM-853 against brain injury in experimental animals

Centella asiatica (L.) has many active ingredients with many important roles, including as antioxidant, anti-inflamation and neuroprotectant. Centella asiatica (L.) can reduce inflammatory reactions by inhibiting the activity of TNF-α. Thus, Centella asiatica (L.) is a potential alternative therapy for traumatic brain injury by reducing inflammation via TNF-α expression modulation. This study aimed to determine the effect of Centella asiatica (L.) on serum TNF-α levels in rat model of traumatic brain injury. This study was conducted during the period of July 3-17, 2020 at the LPPT Unit IV, Gajah Mada University. This was a true experimental with post-test only control group study on 35 male wistar rats as the experimental animals. The rats were divided into 5 groups: P1, P2, and traumatic brain injury groups that received Centella asiatica (L.) treatement at 150, 300, and 600mg/kgBW/d doses, respectively. Blood samples were collected after the experimental animals were terminated to assess serum TNF-α levels. Mean TNF-α levels were 60,980±4,057, 76,931±0,698, P3=75,889±0,948, P4=75,868±1,163, and 74,508±1,126 for P1, P2, P3, P4, and P5, respectively. The Kruskal Wallis test results showed a statistically different between groups (p = 0.005). This study shows that Centella asiatica (L.) can decrease serum TNF-α level in rat model of traumatic brain injury.

Download Full-text

Experimental Study of Therapeutic Efficacy of the Topical Preparation «Kourochitin» in Skin Allergy

Letters in Drug Design & Discovery ◽

10.2174/1570180817666200316155643 ◽

2020 ◽

Vol 17 (10) ◽

pp. 1237-1244

Author(s):

Anna Anatolievna Klimovich ◽

Olga Nikolaevna Styshova ◽

Alexander Mikhailovich Popov ◽

Tatiana Vladimirovna Moskvina ◽

Alexander Vasilevich Tsybulsky ◽

...

Keyword(s):

Therapeutic Efficacy ◽

Protective Action ◽

Skin Lesions ◽

Skin Area ◽

Immunological Parameters ◽

Experimental Animals ◽

Allergic Skin ◽

Curative Action ◽

Macrophage Colony ◽

Allergic Contact

Background: The researchers of PIBOC RAS developed the dermo-protective topical drug called «Kourochitin», active substance of which is known quinazoline alkaloid tryptanthrin. In the present work, therapeutic efficacy of this drug in the treatment of allergic dermatosis was evaluated. Methods: Dermo-protective action of «Kourochitin» was studied in tow murine models: 2, 4- dinitrofluorobenzene- induced allergic contact dermatitis (ACD) and imiquimod-induced psoriasis. Results and Discussion: In a model ACD, it was shown that «Kourochitin» exhibits the curative action on pathophysiological, hematological and immunological parameters in ACD. Namely, «Kourochitin» 1) reduces the level of erythema in the allergen damaged skin area and increases the healing index of the epidermis; 2) normalizes the content of eosinophils, basophils and monocytes in the blood of experimental animals; 3) inhibits the production of main pro-inflammatory cytokines: interleukins - 1 and 2, interferon-gamma, and granulocyte-macrophage colony-stimulating factor. In a murine model of imiquimod-induced psoriasis, it was shown that «Kourochitin» application led to reduction in psoriasis severity on the inflamed epidermis of experimental animals. Additionally, in veterinary research, «Kourochitin»-treatment of canine atopic dermatitis almost completely eliminated signs of allergic manifestations on the epidermis. Conclusion: The obtained data suggest that «Kourochitin» as anti-inflammatory, anti-allergic, and wound healing remedy is a potential drug for therapy of various dermatological diseases, in particular allergic skin lesions.

Download Full-text

A neuroprotective role of the NMDA receptor subunit GluN3A (NR3A) in ischemic stroke of the adult mouse

AJP Cell Physiology ◽

10.1152/ajpcell.00353.2014 ◽

2015 ◽

Vol 308 (7) ◽

pp. C570-C577 ◽

Cited By ~ 13

Author(s):

Jin Hwan Lee ◽

Zheng Z. Wei ◽

Dongdong Chen ◽

Xiaohuan Gu ◽

Ling Wei ◽

...

Keyword(s):

Brain Injury ◽

Cerebral Ischemia ◽

Focal Cerebral Ischemia ◽

Protective Action ◽

Adult Brain ◽

Expression Level ◽

Terminal Deoxynucleotidyl Transferase ◽

Tunel Staining ◽

Triphenyltetrazolium Chloride ◽

Nmdar Subunit

GluN3A or NR3A is a developmentally regulated N-methyl-d-aspartate receptor (NMDAR) subunit, showing a unique inhibitory role that decreases NMDAR current and the receptor-mediated Ca2+ influx. In the neonatal brain, GluN3A is shown to associate with synaptic maturation and spine formation and plays a neuroprotective role. Its functional role in the adult brain, however, is largely unknown. We tested the hypothesis that, disrespecting the relatively lower expression level of GluN3A in the adult brain, this inhibitory NMDAR subunit shows a protective action against ischemia-induced brain injury. In littermate wild-type (WT) and GluN3A knockout (KO) mice, focal cerebral ischemia was induced by permanent occlusion of right distal branches of the middle cerebral artery (MCA) plus 10-min ligation of both common carotid arteries (CCAs). Twenty-four hours after focal cerebral ischemia, the infarction volume assessed using 2,3,5-triphenyltetrazolium chloride (TTC) staining was significantly larger in GluN3A KO mice compared with WT mice. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining demonstrated enhanced cell death in GluN3A KO mice. Moreover, the deletion of GluN3A hindered sensorimotor functional recovery after stroke. It is suggested that, although the expression level is relatively lower in the adult brain, GluN3A is still a noteworthy regulator in ischemia-induced excitotoxicity and brain injury.

Download Full-text

Effect of neural stem cell transplantation on cognitive functions of mice after cerebral ischemia-reperfusion

Cell and Organ Transplantology ◽

10.22494/cot.v1i1.51 ◽

2013 ◽

Vol 1 (1) ◽

pp. 92-95 ◽

Cited By ~ 1

Author(s):

O. Tsupykov ◽

V. Kyryk ◽

O. Rybachuk ◽

P. Poberezhnyi ◽

A. Mamchur ◽

...

Keyword(s):

Brain Injury ◽

Cerebral Ischemia ◽

Cognitive Functions ◽

Neural Progenitor Cells ◽

Ischemia Reperfusion ◽

Global Cerebral Ischemia ◽

Ischemic Brain Injury ◽

Short Term ◽

Ischemic Brain ◽

Experimental Animals

This study is aimed to determine the effect of transplantation of neural progenitor cells (NPCs) isolated from fetal hippocampus on cognitive functions of experimental animals after short-term global cerebral ischemia. NPCs were isolated from hippocampus of FVB-Cg-Tg(GFPU)5Nagy/J mice, transgenic by the GFP. Ischemic brain injury in FVB “wild” type mice was modeled by bilateral occlusion of the common carotid arteries for 20 min. GFP-positive NPCs were stereotaxically transplanted into the hippocampus of experimental animals in 24 hours after ischemia-reperfusion. Cognitive functions were evaluated using Morris water maze. Results of this study showed that global short-term cerebral ischemia resulted into cognitive impairments in mice. Stereotaxic transplantation of NPCs promoted the cognitive function recovery in experimental animals after ischemic brain injury. Thus, the data indicates that transplantation of NPCs may have a therapeutic effect in treating of ischemic stroke.

Download Full-text

THE TREATMENT OF TRAUMATIC BRAIN INJURY IN EXPERIMENTAL ANIMALS BY PYRIMIDINE DERIVATIVES.

10.21474/ijar01/8700 ◽

2019 ◽

Vol 7 (3) ◽

pp. 799-803 ◽

Cited By ~ 1

Author(s):

VoronkovA V ◽

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Pyrimidine Derivatives ◽

Experimental Animals

Download Full-text

Clinical Perspective on Modeling of Traumatic Brain Injury in Aged Experimental Animals

Archives of Physical Medicine and Rehabilitation ◽

10.1016/j.apmr.2017.08.457 ◽

2017 ◽

Vol 98 (10) ◽

pp. e140

Author(s):

Aiwane Iboaya ◽

Randolph Nudo ◽

Janna Harris ◽

Alexandra Nielsen

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Clinical Perspective ◽

Experimental Animals

Download Full-text

Neuroprotective and Neurological/Cognitive Enhancement Effects of Curcumin after Brain Ischemia Injury with Alzheimer’s Disease Phenotype

International Journal of Molecular Sciences ◽

10.3390/ijms19124002 ◽

2018 ◽

Vol 19 (12) ◽

pp. 4002 ◽

Cited By ~ 13

Author(s):

Ryszard Pluta ◽

Marzena Ułamek-Kozioł ◽

Stanisław Czuczwar

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Brain Injury ◽

Brain Ischemia ◽

Tau Protein ◽

Protective Action ◽

Ischemic Brain Injury ◽

Disease Phenotype ◽

Ischemic Brain ◽

Ca1 Region

In recent years, ongoing interest in ischemic brain injury research has provided data showing that ischemic episodes are involved in the development of Alzheimer’s disease-like neuropathology. Brain ischemia is the second naturally occurring neuropathology, such as Alzheimer’s disease, which causes the death of neurons in the CA1 region of the hippocampus. In addition, brain ischemia was considered the most effective predictor of the development of full-blown dementia of Alzheimer’s disease phenotype with a debilitating effect on the patient. Recent knowledge on the activation of Alzheimer’s disease-related genes and proteins—e.g., amyloid protein precursor and tau protein—as well as brain ischemia and Alzheimer’s disease neuropathology indicate that similar processes contribute to neuronal death and disintegration of brain tissue in both disorders. Although brain ischemia is one of the main causes of death in the world, there is no effective therapy to improve the structural and functional outcomes of this disorder. In this review, we consider the promising role of the protective action of curcumin after ischemic brain injury. Studies of the pharmacological properties of curcumin after brain ischemia have shown that curcumin has several therapeutic properties that include anti-excitotoxic, anti-oxidant, anti-apoptotic, anti-hyperhomocysteinemia and anti-inflammatory effects, mitochondrial protection, as well as increasing neuronal lifespan and promoting neurogenesis. In addition, curcumin also exerts anti-amyloidogenic effects and affects the brain’s tau protein. These results suggest that curcumin may be able to serve as a potential preventive and therapeutic agent in neurodegenerative brain disorders.

Download Full-text