Neuroprotective Effects of Ethanol Extract (EEPG) Against Glutamate Induced Neurotoxicity in HT22 Cells.

Oxidative stress induced by glutamate is a significant contributor to neuronal cell damage and can lead to neurodegenerative diseases such as Alzheimer's, Huntington's, and ischemic brain injury. At the cellular level, oxidative stress increases Ca ion influx and reactive oxygen species (ROS), which activate the MAPK signaling pathway. Additionally, the generation of ROS causes mitochondrial dysfunction, triggering apoptosis by promoting the translocation of AIF to the nucleus from the mitochondria.

Lactobacillus fermentum attenuates the alveolar bone loss in ligature-induced periodontitis in mice.

Objective: This study investigated the effects of Lactobacillus fermentum BELF11 on periodontitis in mice (LIP).

Methods: Sixty mice were randomly assigned to a control group (CTL), LIP/PBS group (LIP and PBS applied), or LIP/BELF11 group (LIP and L. fermentum BELF11 applied).

Tat-CIAPIN1 Prevents Pancreatic β-Cell Death in hIAPP-Induced RINm5F Cells and T2DM Animal Model.

It is well known that the cytokine-induced apoptosis inhibitor 1 (CIAPIN1) protein plays an important role in biological progresses as an anti-apoptotic protein. Human islet amyloid peptide (hIAPP), known as amylin, is caused to pancreatic β-cell death in type 2 diabetes mellitus (T2DM). However, the function of CIAPIN1 protein on T2DM is not yet well studied.

Neuroprotective Effects of Ethanol Extract of (EEPF) against Glutamate-Mediated Neuronal Toxicity in HT22 Cells.

In traditional herbal medicine, the has been frequently used for the treatment of ischemia and inflammation. Oxidative stress mediated by elevated glutamate levels cause neuronal cell death in ischemia and various neurodegenerative diseases. However, so far, the neuroprotective effects of this plant extract against glutamate-mediated cell death have not been investigated in cell models.

Synthesis and neuroprotective effects of HS-donor-peptide hybrids on hippocampal neuronal cells.

Hydrogen sulfide (HS) has emerged as an endogenous signaling molecule that functions in many physiological and pathological processes of human cells in health and disease, including neuromodulation and neuroprotection, inflammation, angiogenesis, and vasorelaxation. The limited clinical applications of current HS donors have led to the development of HS donor hybrid compounds that combine current HS donors with bioactive molecules. Finely tuned multi-targeting hybrid molecules have been shown to have complementary neuroprotective effects against reactive oxygen species (ROS)-induced oxidative stress.

Temporal changes of periodontal tissue pathology in a periodontitis animal model.

Purpose: This study aimed to characterize the early stages of periodontal disease and determine the optimal period for its evaluation in a mouse model. The association between the duration of ligation and its effect on the dentogingival area in mice was evaluated using micro-computed tomography (CT) and histological analysis.

Methods: Ninety mice were allocated to an untreated control group or a ligation group in which periodontitis was induced by a 6-0 silk ligation around the left second maxillary molar.

Application time and persistence of transcranial direct current stimulation (tDCS) against neuronal death resulting from transient cerebral ischemia.

Background: Transcranial direct current stimulation (tDCS) has been studied as a tool to stimulate the functional recovery of neurons after stroke. Although this device has recently begun to be utilized for providing neuroprotection in stroke, research on its application conditions is lacking. This study aimed to examine the effects of various tDCS application conditions on cerebral ischemia.

The Effect of Botulinum Toxin on Hair Follicle Cell Regeneration Under Continuous Stress Conditions: a Pilot Animal Study.

We analyzed the effect of botulinum toxin (BTX) type A on the regeneration of hair follicle cells under continuous stress conditions. Thirty 6-week-old C57BL/6 mice were used, and hair loss was induced on their backs (10 control (CTL) mice, reared under normal conditions without stress; 10 mice, exposed to continuous stress (STRESS) by fixing in an enclosed space; 10 BTX + STRESS mice, injected subcutaneously with 1 IU of BTX (0.1 cc) where the hair follicles were removed under the same stress conditions).

Effects of ibuprofen-loaded TiO₂ nanotube dental implants in alloxan-induced diabetic rabbits.

Purpose: Some systemic conditions, especially diabetes mellitus (DM), adversely affect dental implant success. This study aimed to investigate the effects of ibuprofen-loaded TiO nanotube (ILTN) dental implants in alloxan-induced diabetic rabbits.

Methods: Twenty-six New Zealand white rabbits were treated with alloxan monohydrate to induce DM.

Neuroprotective effects of 2-heptyl-3-hydroxy-4-quinolone in HT22 mouse hippocampal neuronal cells.

The neuroprotective activity of 2-heptyl-3-hydroxy-4(1H)-quinolone (compound 1) was evaluated using the neurotoxicity of glutamate in the HT22 cell line. Compound 1, known as a signal molecule of the bacterial quorum-sensing system, protects neuronal cells from glutamate-induced neurotoxicity by inhibiting cellular Ca uptake and glutamate-triggered ROS accumulation. MAPK signaling pathway inhibition by compound 1 was evaluated by immunoblotting the phosphorylation status of the proteins.

Effect of Weissella cibaria on the reduction of periodontal tissue destruction in mice.

Background: Periodontitis is associated with dysbiosis of microbial flora in the oral cavity. We evaluated the effects of an oral care probiotic, Weissella cibaria CMU, on periodontal tissue destruction and regulation of inflammatory cytokines in mice with ligature-induced periodontitis (LIP).

Methods: Fourteen-day LIP model was used.

Determination of the optimal diabetes duration for bone regeneration experiments in an alloxan-induced diabetic rabbit calvarial defect model.

Purpose: The purpose of this study was to evaluate the optimal diabetes duration for bone regeneration experiments in an alloxan monohydrate (ALX)-induced diabetic rabbit calvarial defect model by evaluating the association between diabetes duration and bone healing capacity.

Methods: Twenty-four New Zealand white rabbits were used. Twenty-two rabbits were injected with 100 mg/kg of ALX to induce experimental diabetes.

Effects of silk solution against laminectomy-induced dural adhesion formation and inflammation in a rat model.

The authors investigated the effects of a silk solution against laminectomy-induced dural adhesion formation and inflammation in a rat model. They found that it significantly reduced postlaminectomy dural adhesion formation and inflammation. Dural adhesion formation, thought to be an inevitable consequence of laminectomy, is one of the most common complications following spinal surgery, and the authors' results indicate that the silk solution might be a potential novel therapeutic agent for dural adhesion formation.

Extract Promotes Neurogenesis in the Hippocampal Dentate Gyrus of the Adult Mouse through Increasing Expressions of Brain-Derived Neurotrophic Factor and Tropomyosin-Related Kinase B.

Background: Glehnia littoralis has been used for traditional Asian medicine, which has diverse therapeutic activities. However, studies regarding neurogenic effects of G. littoralis have not yet been considered.

Determination of the critical diabetes duration in a streptozotocin-induced diabetic rat calvarial defect model for experimentation regarding bone regeneration.

Purpose: The purpose of this study was to determine the critical diabetes duration in a streptozotocin (STZ)-induced diabetic rat calvarial defect model for experimentation regarding bone regeneration by evaluating the association between diabetes duration and bone healing capacity through histological and radiographic analyses.

Methods: Experimental diabetes was induced in 50 of 60 rats by an STZ injection. The rats were divided into 5 groups, including a control group (group 1), according to diabetes durations of 0, 2, 4, 6, and 8 weeks, respectively.

CD74-immunoreactive activated M1 microglia are shown late in the gerbil hippocampal CA1 region following transient cerebral ischemia.

Activated M1 microglia secrete proinflammatory cytokines into damaged brain areas. The present study examined activated M1 microglial morphology and expression in the hippocampal Cornu Ammonis (CA) 1 region, which is vulnerable to transient ischemia. Transient cerebral ischemia was performed for 5 min in gerbils, and neuronal death in the CA1 region following transient cerebral ischemia was confirmed using cresyl violet staining, neuronal nuclear antigen immunohistochemistry and Fluoro‑Jade B histofluorescent staining.

Essential oils from two Allium species exert effects on cell proliferation and neuroblast differentiation in the mouse dentate gyrus by modulating brain-derived neurotrophic factor and acetylcholinesterase.

Background: In the present study, we investigated the effects of oil products from two Allium species: Allium sativum (garlic) and Allium hookeri (Chinese chives) on cell proliferation and neuroblast differentiation in the mouse dentate gyrus.

Methods: Using corn oil as a vehicle, the essential oil from garlic (10 ml/kg), or Chinese chives (10 ml/kg) was administered orally to 9-week-old mice once a day for 3 weeks. One hour following the last treatment, a novel object recognition test was conducted and the animals were killed 2 h after the test.

Hydroquinone Strongly Alleviates Focal Ischemic Brain Injury via Blockage of Blood-Brain Barrier Disruption in Rats.

Hydroquinone (HQ), a major benzene metabolite, occurs naturally in various plants and is manufactured for commercial use. Although HQ displays various biological effects, its neuroprotective effects following ischemic insults have not been investigated. In this study, we first examined neuroprotective effects of HQ in a rat model of transient focal cerebral ischemia.

Time- and cell-type specific changes in iron, ferritin, and transferrin in the gerbil hippocampal CA1 region after transient forebrain ischemia.

In the present study, we used immunohistochemistry and western blot analysis to examine changes in the levels and cellular localization of iron, heavy chain ferritin (ferritin-H), and transferrin in the gerbil hippocampal CA1 region from 30 minutes to 7 days following transient forebrain ischemia. Relative to sham controls, iron reactivity increased significantly in the stratum pyramidale and stratum oriens at 12 hours following ischemic insult, transiently decreased at 1-2 days and then increased once again within the CA1 region at 4-7 days after ischemia. One day after ischemia, ferritin-H immunoreactivity increased significantly in the stratum pyramidale and decreased at 2 days.

Aronia melanocarpa Concentrate Ameliorates Pro-Inflammatory Responses in HaCaT Keratinocytes and 12-O-Tetradecanoylphorbol-13-Acetate-Induced Ear Edema in Mice.

Abnormal expression of pro-inflammatory mediators such as cell adhesion molecules and cytokines has been implicated in various inflammatory skin diseases, including atopic dermatitis. In this study, we investigated the anti-inflammatory activity of Aronia melanocarpa concentrate (AC) and its action mechanisms using in vivo and in vitro skin inflammation models. Topical application of AC on mouse ears significantly suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema formation, as judged by measuring ear thickness and weight, and histological analysis.

Neuroprotection of Chrysanthemum indicum Linne against cerebral ischemia/reperfusion injury by anti-inflammatory effect in gerbils.

In this study, we tried to verify the neuroprotective effect of Chrysanthemum indicum Linne (CIL) extract, which has been used as a botanical drug in East Asia, against ischemic damage and to explore the underlying mechanism involving the anti-inflammatory approach. A gerbil was given CIL extract for 7 consecutive days followed by bilateral carotid artery occlusion to make a cerebral ischemia/reperfusion model. Then, we found that CIL extracts protected pyramidal neurons in the hippocampal CA1 region (CA1) from ischemic damage using neuronal nucleus immunohistochemistry and Fluoro-Jade B histofluorescence.

Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus After Ischemic Stroke.

Background: The positive correlation between therapeutic exercise and memory recovery in cases of ischemia has been extensively studied; however, long-term exercise begun after ischemic neuronal death as a chronic neurorestorative strategy has not yet been thoroughly examined.

Objective: The purpose of this study is to investigate possible mechanisms by which exercise ameliorates ischemia-induced memory impairment in the aged gerbil hippocampus after transient cerebral ischemia.

Methods: Treadmill exercise was begun 5 days after ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks.

Oenanthe Javanica Extract Protects Against Experimentally Induced Ischemic Neuronal Damage via its Antioxidant Effects.

Background: Water dropwort (Oenanthe javanica) as a popular traditional medicine in Asia shows various biological properties including antioxidant activity. In this study, we firstly examined the neuroprotective effect of Oenanthe javanica extract (OJE) in the hippocampal cornus ammonis 1 region (CA1 region) of the gerbil subjected to transient cerebral ischemia.

Methods: Gerbils were established by the occlusion of common carotid arteries for 5 min.

New GABAergic Neurogenesis in the Hippocampal CA1 Region of a Gerbil Model of Long-Term Survival after Transient Cerebral Ischemic Injury.

We investigated the probability of newly generated neurons that could survive and mature in the ischemic hippocampal CA1 region (CA1) of a gerbil model of transient cerebral ischemia. Neuronal death was shown in the stratum pyramidale (SP) from 4 days post-ischemia, and a significant increase in NeuN-positive ((+) ) neurons was found in the SP at 180 days post-ischemia. 5-Bromo-2-deoxyuridine (BrdU)(+) cells were co-stained with NeuN and glutamic decarboxylase 67 (GAD67).

Ischemic preconditioning protects hippocampal pyramidal neurons from transient ischemic injury via the attenuation of oxidative damage through upregulating heme oxygenase-1.

Ischemic preconditioning (IPC) provides neuroprotection against subsequent severe ischemic injury by activating specific mechanisms. In this study, we tested the hypothesis that IPC attenuates postischemic neuronal death via heme oxygenase-1 (HO-1). Animals used in this study were randomly assigned to 4 groups; sham-operated group, ischemia-operated group, IPC plus (+) sham-operated group and IPC+ischemia-operated group.