Anti-Oxidant Activity of Gallotannin-Enriched Extract of Galla Rhois Can Associate with the Protection of the Cognitive Impairment through the Regulation of BDNF Signaling Pathway and Neuronal Cell Function in the Scopolamine-Treated ICR Mice

Abstract

The antibacterial, anti-inflammatory, anti-metastatic/anti-invasion activities and laxative activity of Galla Rhois (GR) are well-known, although the neuropreservation effects of their extracts are still to be elucidated. To investigate the novel therapeutic effects and molecular mechanism of GR on alleviation of cognitive impairment, two different dosages of gallotannin-enriched GR (GEGR) were administered to Korl:ICR mice for three weeks, and to induce memory impairment, scopolamine (SP) was administered during the last seven days of the GEGR treatment period. GEGR showed the high level of the free radical scavenging activity to DPPH and suppressive activity to reactive oxygen species (ROS) in B35 cells as well as enhanced SOD and CAT activity in brains of the SP-induced model. Latency time for memory impairment assessed by the passive avoidance test significantly protected in the SP+GEGR treated group as compared to the SP+Vehicle treated group. Moreover, similar protective effects were observed on the secretion of BDNF in SP+GEGR treated mice. The expression of TrkB receptor, and phosphorylation of PI3K on the TrkB receptor signaling pathway were dramatically protected in the SP-induced model after GEGR treatment, whereas the expression of p75NTR receptor, the phosphorylation of JNK, and expression of Bax/Bcl-2 on the p75NTR receptor signaling pathway was significantly protected in the same group. Furthermore, the GEGR treated SP-induced model showed decreased number of dead neural cells and suppressed acetylcholine esterase (AChE) activity and inhibited inflammatory responses. Taken together, these results indicate that the anti-oxidant activity of GEGR contributes to improving the neuronal cell function and survival during cognitive impairment in the SP-induced model through regulation of BDNF secretion and their receptor signaling pathway.

Protective Effects of the Soluble Epoxide Hydrolase Inhibitor 1-Trifluoromethoxyphenyl-3-(1-Propionylpiperidin-4-yl) Urea in a Rat Model of Permanent Middle Cerebral Artery Occlusion

“…While overexpression of SEH increased cell death. These datas were also in agreement with previous reports that protecting endothelial cells and neurons from pro-inflammatory mediators induced apoptosis by MAPK or PI3/Akt or BDNF signaling pathway in ischemic brain tissue (Hung et al, 2017;Hao et al, 2018;Park et al, 2019). We speculate that TPPU may exert this effect by reducing ischemia-induced mitochondrial damage and therefore mitochondria-mediated apoptotic signaling (Rekuviene et al, 2017).…”

Mechanisms of Oxidative Stress and Therapeutic Targets following Intracerebral Hemorrhage

“…Hematomal and perihematomal regions are biochemically active environments that sustain oxidative damage following ICH [ 2 ]. OS is defined as an imbalance between the formation of strong oxidants and physiologic antioxidant capacity [ 3 ]. ROS such as oxygen free radicals (e.g., superoxide (O 2 − ) and hydroxyl radicals (OH − )) and nonradical compounds (e.g., hydrogen peroxide (H 2 O 2 ) and hypochlorous acid), as well as reactive nitrogen species (RNS; e.g., nitric oxide (NO)) and a variety of nitrogenous compounds produced as metabolic byproducts, are the major drivers of oxidative damage [ 4 ] to proteins, lipids, and nucleic acids, which can induce inflammation, autophagy, apoptosis, and destruction of the BBB.…”

A Multifunctional (-)-Meptazinol-Serotonin Hybrid Ameliorates Oxidative Stress-Associated Apoptotic Neuronal Death and Memory Deficits via Activating the Nrf2/Antioxidant Enzyme Pathway

“…Moreover, it causes oxidative stress and promotes neuronal apoptosis [15,44,45]. Therefore, scopolamine has been applied in animal models to elicit AD-like symptoms involving both cholinergic dysfunction and oxidative stress [15,18]. We first performed behavioral experiments using the Morris water maze test to detect the effect of Mep-S in scopolamine-challenged mice.…”

“…Considering the critical roles of oxidative stress in AD pathogenesis, MTDLs with antioxidant potency may be favorable for AD therapy. In fact, the development of anti-AD MTDLs with antioxidant activity has recently attracted much attention [15,18]. In a previous research, we reported a number of (-)-meptazinol-melatonin/serotonin hybrids with multiple pharmacological properties [19].…”