Electroacupuncture pre-treatment ameliorates PTSD symptoms in rats by enhancinghippocampal neurogenesis via the Nrf2 antioxidant signal pathway

2019 ◽  
Vol 12 (2) ◽  
pp. 416
Author(s):  
C. Zhou ◽  
S. Xue ◽  
Z. Peng ◽  
H. Wang
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi-An Lin ◽  
Yan-Rong Li ◽  
Yi-Ching Chang ◽  
Mei-Chich Hsu ◽  
Szu-Tah Chen

AbstractThe regenerative effect of Epimedium and its major bioactive flavonoid icariin (ICA) have been documented in traditional medicine, but their effect on sarcopenia has not been evaluated. The aim of this study was to investigate the effects of Epimedium extract (EE) on skeletal muscle as represented by differentiated C2C12 cells. Here we demonstrated that EE and ICA stimulated C2C12 myotube hypertrophy by activating several, including IGF-1 signal pathways. C2C12 myotube hypertrophy was demonstrated by enlarged myotube and increased myosin heavy chains (MyHCs). In similar to IGF-1, EE/ICA activated key components of the IGF-1 signal pathway, including IGF-1 receptor. Pre-treatment with IGF-1 signal pathway specific inhibitors such as picropodophyllin, LY294002, and rapamycin attenuated EE induced myotube hypertrophy and MyHC isoform overexpression. In a different way, EE induced MHyC-S overexpression can be blocked by AMPK, but not by mTOR inhibitor. On the level of transcription, EE suppressed myostatin and MRF4 expression, but did not suppress atrogenes MAFbx and MuRF1 like IGF-1 did. Differential regulation of MyHC isoform and atrogenes is probably due to inequivalent AKT and AMPK phosphorylation induced by EE and IGF-1. These findings suggest that EE/ICA stimulates pathways partially overlapping with IGF-1 signaling pathway to promote myotube hypertrophy.


Author(s):  
Lisa M. Linning ◽  
Christopher Kearney

Therapy to address PTSD symptoms in maltreated youth has received increased research attention in recent years.  However, little data are available regarding the treatment of youth temporarily housed in shelter care facilities whose parents are unavailable or inaccessible.  The present study examined a brief group therapy protocol for such youth in a county-operated shelter.  Participants received 1-6 sessions of treatment depending on their length of stay at the shelter.  Treatment components included psychoeducation, anxiety management, cognitive restructuring and coping skills, emotional expression, mindfulness, brief exposure, boundary setting, and journaling.  Results revealed a significant reduction in PTSD symptoms overall and that number of group therapy sessions mediated pre-treatment and post-treatment scores on various dependent measures.  In addition, level of pre-treatment dissociation predicted reduction in PTSD levels.  These preliminary results indicate that brief treatment for youth temporarily housed in a shelter care facility can provide some amelioration of PTSD-related symptoms.


2021 ◽  
Vol 10 (8) ◽  
pp. 1553
Author(s):  
Harmen A. Zoet ◽  
Ad de Jongh ◽  
Agnes van Minnen

For patients with complex or other severe forms of PTSD, particularly in cases with dissociative symptoms, different treatment approaches have been suggested. However, the influence of somatoform dissociation on the effectiveness of trauma-focused treatment has hardly ever been studied. This study aims to test the hypotheses that (1) PTSD patients reporting a low level and those reporting a high level of somatoform dissociative symptoms would both benefit from an intensive trauma-focused treatment, and that (2) somatoform dissociative symptoms would alleviate. Participants were 220 patients with severe PTSD, enrolled in an intensive treatment program combining EMDR therapy and prolonged exposure therapy, without a preceding stabilization phase. Trauma history was diversified, and comorbidity was high. PTSD symptoms (CAPS-5 and PCL-5) and somatoform dissociative symptoms (SDQ-5 and SDQ-20) were assessed at pre-treatment, post-treatment and at six months after completion of treatment. The course of both PTSD and somatoform dissociative symptoms was compared for individuals reporting low and for those reporting high levels of somatoform dissociative symptoms. Large effect sizes were observed regarding PTSD symptoms reduction for patients with both low and high levels of somatoform dissociation. Somatoform dissociation did not impact improvement in terms of PTSD symptom reduction. The severity of somatoform dissociative symptoms decreased significantly in both groups. This decrease was greater for those with a positive screen for a dissociative disorder. These results add further support to the notion that the presence of strong somatoform dissociative symptoms in patients with PTSD does not necessarily call for a different treatment approach. Clinical implications are discussed.


Author(s):  
E Y. Wang ◽  
J. T. Cherian ◽  
A. Madsen ◽  
R. M. Fisher

Many steel parts are electro-plated with chromium to protect them against corrosion and to improve their wear-resistance. Good adhesion of the chrome plate to the steel surface, which is essential for long term durability of the part, is extremely dependent on surface preparation prior to plating. Recently, McDonnell Douglas developed a new pre-treatment method for chrome plating in which the steel is anodically etched in a sulfuric acid and hydrofluoric acid solution. On carbon steel surfaces, this anodic pre-treatment produces a dark, loosely adhering material that is commonly called the “smut” layer. On stainless steels and nickel alloys, the surface is only darkened by the anodic pre-treatment and little residue is produced. Anodic pre-treatment prior to hard chrome plating results in much better adherence to both carbon and alloy steels.We have characterized the anodic pre-treated steel surface and the resulting “smut” layer using various techniques including electron spectroscopy for chemical analysis (ESCA) on bulk samples and transmission electron microscopy (TEM) and electron energy-loss spectroscopy (EELS) on stripped films.


2021 ◽  
Vol 160 (1) ◽  
pp. 234-243
Author(s):  
Diana Samoil ◽  
Nazek Abdelmutti ◽  
Lisa Ould Gallagher ◽  
Nazlin Jivraj ◽  
Naa Kwarley Quartey ◽  
...  

2004 ◽  
Vol 74 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Liu ◽  
Russell ◽  
Smith ◽  
Bronson ◽  
Milbury ◽  
...  

Because reactive oxygen species have been implicated as mediators of inflammatory bowel disease (IBD), we evaluated the potential preventive and therapeutic effects of two dietary antioxidants, glutathione (GSH) and coenzyme Q10 (CoQ10) on dextran sulfate sodium (DSS)-induced colitis in mice. Fifty female 8-wk old Swiss-Webster mice were randomly assigned to 4 groups for a pre-treatment 'prevention' study: (1) GSH (1% of diet); (2) CoQ10 (200 mg/kg/d); (3) DSS only (3% of drinking water); (4) control (no treatment). The mice in groups 1 and 2 were fed with GSH or CoQ10 for 21 wks, and the mice in groups 1, 2 and 3 were provided DSS from wk 7 for 4 cycles (1 cycle = 1 wk DSS followed by 2-wk water). Another 50 mice were randomly assigned to 4 groups for a 21-wk 'treatment' study where the mice in groups 1, 2, and 3 were administered DSS for 6 cycles (18 wks) to induce colitis. GSH and CoQ10 were added from wk 7 until the completion of the protocol. Loose stools and hemocult positivity were modestly but significantly reduced with GSH or CoQ10 at several periods during the intervention in both the prevention and treatment studies. In contrast, histological evaluation revealed increases in colonic dysplasia and ulceration with GSH or CoQ10. Thus, in this mouse model, GSH and CoQ10 appear to have a beneficial effect on acute signs of IBD, but may have an adverse impact on the chronic pathophysiology of the disease. Further studies using additional animal models are required to determine whether GSH or CoQ10 provide a favorable or unfavorable benefit:risk ratio in the prevention or treatment of IBD.


2014 ◽  
Vol 84 (3-4) ◽  
pp. 0140-0151 ◽  
Author(s):  
Thilaga Rati Selvaraju ◽  
Huzwah Khaza’ai ◽  
Sharmili Vidyadaran ◽  
Mohd Sokhini Abd Mutalib ◽  
Vasudevan Ramachandran ◽  
...  

Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100 - 300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76 % and 79 % in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2 %, 95.0 %, and 95.6 %, respectively (p < 0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.


2010 ◽  
Vol 218 (2) ◽  
pp. 135-140 ◽  
Author(s):  
Slawomira J. Diener ◽  
Herta Flor ◽  
Michèle Wessa

Impairments in declarative memory have been reported in posttraumatic stress disorder (PTSD). Fragmentation of explicit trauma-related memory has been assumed to impede the formation of a coherent memorization of the traumatic event and the integration into autobiographic memory. Together with a strong non-declarative memory that connects trauma reminders with a fear response the impairment in declarative memory is thought to be involved in the maintenance of PTSD symptoms. Fourteen PTSD patients, 14 traumatized subjects without PTSD, and 13 non-traumatized healthy controls (HC) were tested with the California Verbal Learning Test (CVLT) to assess verbal declarative memory. PTSD symptoms were assessed with the Clinician Administered PTSD Scale and depression with the Center of Epidemiological Studies Depression Scale. Several indices of the CVLT pointed to an impairment in declarative memory performance in PTSD, but not in traumatized persons without PTSD or HC. No group differences were observed if recall of memory after a time delay was set in relation to initial learning performance. In the PTSD group verbal memory performance correlated significantly with hyperarousal symptoms, after concentration difficulties were accounted for. The present study confirmed previous reports of declarative verbal memory deficits in PTSD. Extending previous results, we propose that learning rather than memory consolidation is impaired in PTSD patients. Furthermore, arousal symptoms may interfere with successful memory formation in PTSD.


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