scholarly journals Antiaging, Cognition and Anti-Inflammatory Potential of the Biofield Energy Treatment in Vitamin D3 Deficiency Diet (VDD) Induced Sprague Dawley Rats

2020 ◽  
Vol 3 (4) ◽  
Author(s):  
Snehasis Jana
Keyword(s):  
Vitamin D3 ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Anti Inflammatory ◽  
Vitamin D3 Deficiency

Evaluation of Vitamin D3 metabolite (25-OH Vit D3), Neurotransmitter (ACh), and the Expression of Proinflammatory Cytokines (IL-6 and TNF-α) in Tissue Homogenate after Administration of Biofield Energy Healing-based Novel Proprietary Test Formulation and Biofield Treatment per se to the Animals in Vitamin D3 Deficiency Diet (VDD)-induced Sprague Dawley Rats

2021 ◽  
Vol 3 (4) ◽  
pp. 1-11
Author(s):  
Mahendra Kumar Trivedi ◽  
Alice Branton ◽  
Dahryn Trivedi ◽  
Snehasis Jana
Keyword(s):  
Disease Control ◽  
Proinflammatory Cytokines ◽  
Vitamin D3 ◽  
Sprague Dawley ◽  
Test Formulation ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Per Se ◽  
Vitamin D3 Metabolite ◽  
Vitamin D3 Deficiency

A novel proprietary test formulation was designed which included minerals, vitamins, β-carotene, cannabidiol isolate,and Panax ginseng extract. This present study was evaluated the impact of the Trivedi Effect® on novel proprietary test formulation in male Sprague Dawley rats, fed with vitamin D3 deficiency diet (VDD). The novel test formulation was divided into two parts; one part was defined as untreated test formulation, while the other part was defined as the Biofield Energy Treated sample, which received the Biofield Energy Healing Treatment by renowned Biofield Energy Healer, Mr. Mahendra Kumar Trivedi. The level of 25-OH Vit. D3 was measured in brain homogenate, which was found to be increased by 20.13%, 24.12%, 45.86%, 14.79%, and 29.96% in the G5 group treated with Biofield Treated test formulation, Biofield Energy Treatment per se to the animals (G6), 15 days pre-treatment of Biofield Energy Treated test formulation (G7), Biofield Energy Treatment per se plus Biofield Energy Treated test formulation from day -15 (G8), and untreated test formulation to the Biofield Energy Treated animals (G9) groups respectively, as compared with the disease control (G2) group. Brain acetylcholine (ACh) level was increased by 61.33% in the G7 group as compared with the untreated test formulation (G4) group. The expression of interleukin-6 (IL-6) was significantly reduced by 43.44% (p≤0.01), 30.93%, 21.42%, 45.99% (p≤0.01), and 60.85% (p≤0.01), respectively as compared with the G4. Lung pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) level was significantly reduced in the G5, G6, G7, and G8 by 24.86%, 32.55% (p≤0.01), 30.12% (p≤0.01), and 42.69% (p≤0.01), respectively, as compared with the G4 group. Altogether, the Biofield Treated test formulation and/or per se treatment to the animals significantly improved the levels of active form of vitamin D3 metabolite (25-OH Vit D3) and neurotransmitter (ACh); consequently significantly lowered the expression of proinflammatory cytokines (IL-6 and TNF-α). Therefore, the energized test formulation or per se treatment could be effectively useful against neuronal damage and inflammation for the management of brain disorders such as Alzheimer’s disease, dementias, brain cancer, epilepsy and other seizure disorders, mental disorders, and Parkinson’s. Thus, the results showed a significant slowdown of disease progression and all other disease-related complications/symptoms in the preventive Biofield Energy Treatment group per se and the Biofield Energy Treated Test formulation groups (viz. G6, G7, G8, and G9) as compared to the disease control group.

scholarly journals Levosimendan as a therapeutic strategy to prevent neuroinflammation after aneurysmal subarachnoid hemorrhage?

2021 ◽  
pp. neurintsurg-2021-017504
Author(s):  
Stefan Wanderer ◽  
Lukas Andereggen ◽  
Jan Mrosek ◽  
Sepide Kashefiolasl ◽  
Gerrit Alexander Schubert ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Severe Heart Failure ◽  
Prostaglandin F2alpha ◽  
Sprague Dawley ◽  
Delayed Cerebral Vasospasm ◽  
Sprague Dawley Rats ◽  
Solvent Control ◽  
Anti Inflammatory

BackgroundPoor patient outcomes after aneurysmal subarachnoid hemorrhage (SAH) occur due to a multifactorial process, mainly involving cerebral inflammation (CI), delayed cerebral vasospasm (DCVS), and delayed cerebral ischemia, followed by neurodegeneration. CI is mainly triggered by enhanced synthesis of serotonin (5-HT), prostaglandin F2alpha (PGF2a), and cytokines such as interleukins. Levosimendan (LV), a calcium-channel sensitizer, has already displayed anti-inflammatory effects in patients with severe heart failure. Therefore, we wanted to elucidate its potential anti-inflammatory role on the cerebral vasculature after SAH.MethodsExperimental SAH was induced by using an experimental double-hemorrhage model. Sprague Dawley rats were harvested on day 3 and day 5 after the ictus. The basilar artery was used for isometric investigations of the muscular media tone. Vessel segments were either preincubated with LV or without, with precontraction performed with 5-HT or PGF2a followed by application of acetylcholine (ACh) or LV.ResultsAfter preincubation with LV 10−4 M and 5-HT precontraction, ACh triggered a strong vasorelaxation in sham segments (LV 10−4 M, Emax 65%; LV 10−5 M, Emax 48%; no LV, Emax 53%). Interestingly, SAH D3 (LV 10−4, Emax 76%) and D5 (LV 10−4, Emax 79%) segments showed greater vasorelaxation compared with sham. An LV series after PGF2a precontraction showed significantly enhanced relaxation in the sham (P=0.004) and SAH groups (P=0.0008) compared with solvent control vessels.ConclusionsLV application after SAH seems to beneficially influence DCVS by antagonizing 5-HT- and PGF2a-triggered vasoconstriction. Considering this spasmolytic effect, LV might have a role in the treatment of SAH, additionally in selected patients suffering takotsubo cardiomyopathy.

scholarly journals Activation of cholinergic anti-inflammatory pathway involved in therapeutic actions of α-mangostin on lipopolysaccharide-induced acute lung injury in rats

2020 ◽  
Vol 34 ◽  
pp. 205873842095494
Author(s):  
Zhe Yang ◽  
Qin Yin ◽  
Opeyemi Joshua Olatunji ◽  
Yan Li ◽  
Shu Pan ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Sprague Dawley ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Inflammatory Pathway ◽  
Inflammatory Reactions ◽  
Sprague Dawley Rats ◽  
Anti Inflammatory

Introduction: Alpha-mangostin (MAN) possesses a wide variety of pharmacological effects. In this study, we investigated its effect on cholinergic anti-inflammatory pathway (CAP), and tested if CAP regulation was involved in the therapeutic action on acute lung injury (ALI). Methods: Male Sprague Dawley rats were pre-treated with MAN (40 mg/kg) for 3 days and ALI was induced with an intraperitoneal injection of lipopolysaccharide (LPS). Certain rats received monolateral vagotomy or sham surgery. The effects on inflammatory reactions and relevant pathways in ALI rats or LPS pre-treated RAW 264.7 cells were investigated by histological, immunohistochemical, immunoblotting, RT-qPCR, and immunofluorescence assays, while levels of proinflammatory cytokines, acetylcholine (Ach) and the enzymatic activity of acetylcholinesterase (AchE) were determined by corresponding quantitative kits. Results: Oral administration of MAN reduced the severity of ALI, while vagotomy surgery antagonized this effect. MAN restored the decline in α7 nicotinic acetylcholine receptor (α7nAchR) in the lungs of ALI rats, and promoted the expression of α7nAchR and choline acetyltransferase (CHAT) in RAW 264.7 cells. Although AchE expression was barely affected by MAN at 5 μg/ml, its catalytic activity was reduced by almost 95%. Extracellular rather than intracellular Ach was notably raised shortly after MAN treatment. Furthermore, MAN at 5 μg/ml effectively inhibited LPS-induced increase in phosphorylation and nucleus translocation of p65 subunit, and secretion of TNF-α and IL-1β, which was then offset by methyllycaconitine citrate hydrate. Conclusion: MAN activated CAP by increasing peripheral Ach and up-regulating α7nAchR expression, which eventually led to NF-κB inhibition and remission of acute inflammations.

scholarly journals Anti-inflammatory activity of palmitoylethanolamide ameliorates osteoarthritis induced by monosodium iodoacetate in Sprague–Dawley rats

2021 ◽  
Vol 29 (5) ◽  
pp. 1475-1486
Author(s):  
Jae In Jung ◽  
Hyun Sook Lee ◽  
Young Eun Jeon ◽  
So Mi Kim ◽  
Su Hee Hong ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Acid Amide ◽  
Treatment Strategies ◽  
Leukotriene B4 ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Monosodium Iodoacetate ◽  
Anti Inflammatory

AbstractNovel treatment strategies are urgently required for osteoarthritis (OA). Palmitoylethanolamide (PEA) is a naturally occurring fatty acid amide with analgesic and anti-inflammatory effects. We aimed to examine its effect on OA and elucidate the molecular mechanism of actions in monosodium iodoacetate (MIA)-induced OA Sprague–Dawley rats. The experimental animals were divided into normal control group (injected with saline + treated with phosphate-buffered saline (PBS), NOR), control group (injected with MIA + treated with PBS, CON), 50 or 100 mg/kg body weight (BW)/day PEA-treated group (injected with MIA + treated with 50 or 100 mg of PEA/kg BW/day, PEA50 or PEA100), and positive control group (injected with MIA + treated with 6 mg of diclofenac/kg BW/day, DiC). The changes in blood parameters, body parameters, gene expression of inflammatory mediators and cytokines, knee thickness, and joint tissue were observed. Oral administration of PEA had no adverse effects on the BW, liver, or kidneys. PEA reduced knee joint swelling and cartilage degradation in MIA-induced OA rats. The serum levels of leukotriene B4, nitric oxide, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and prostaglandin E2 considerably reduced in the PEA100 group compared with those in the CON group. In the synovia of knee joints, the mRNA expression of iNOS, 5-Lox, Cox-2, Il-1β, Tnf-α, and Mmp-2, -3, -9, and -13 apparently increased with MIA administration. Meanwhile, Timp-1 mRNA expression apparently decreased in the CON group but increased to the normal level with PEA treatment. Thus, PEA can be an effective therapeutic agent for OA.

scholarly journals Anti-inflammatory activity of aqueous extracts of Ove Costa Rican medicinalplants in Sprague-Dawley rats

2015 ◽  
pp. 723-727
Author(s):  
Beatriz Badilla ◽  
Gerardo Mora ◽  
Luis Jorge Poveda
Keyword(s):  
Costa Rican ◽  
Inflammatory Activity ◽  
Control Group ◽  
Aqueous Extracts ◽  
Paw Edema ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Edema Model ◽  
Anti Inflammatory ◽  
Lethal Doses

The anti-inflamrnatory properties of Loasa specic¡sa and Loasa triphylla (Loasaceae), Urtica leptuphylla and Urera baccifera (Urticaceae), and Chaptalia nutans (Astemceae) were studied using the carregeenan induced mt paw edema model. Aqueous extmcts of each plant were made according to the ethnoboranical use. The hippocratic assay was made with female mts; the dose used was 500 mglkg i.p. andthe control group received 0.5 mi of n.s.s .. A11 the lmimals treated showed hipothermia, and those treated with the extmcts of Chaptalia nutans, Urera baccifera and Urtica lept/lPhylla showed an increased colinergic activity. Acute toxicities of !he aqueous extmcts were studied in mice an tbe mean lethal doses ranged between 1.0226 and 1.2022 glkg. The extracts of Urera baccifera, Chaptalia nutans, Loasa speciosa and Loasa triphylla (500 mglkg i.p.) showed an antiinflarnmatory activity compamble with that of indomethacin. The extracts of U. baccifera and C. nutans, which showed the gI"tatest anti-inflamrtJatory activity, did not show it when used orally (500 mg/k:g p.o.).

scholarly journals ACUTE TOXICITY OF CHITOSAN NANOPARTICLES CONTAINING MAHKOTA DEWA (PHALERIA MACROCARPA) LEAF EXTRACT AND ANTI-INFLAMMATORY EFFECTS IN A DEXTRAN SODIUM SULFATE-INDUCED MOUSE MODEL OF ULCERATIVE COLITIS

2018 ◽  
Vol 10 (1) ◽  
pp. 6
Author(s):  
Ari Estuningtyas ◽  
Santi Widiasari ◽  
Kusmardi Kusmardi
Keyword(s):  
Acute Toxicity ◽  
Leaf Extract ◽  
Chitosan Nanoparticles ◽  
Toxicity Testing ◽  
Inflammatory Cells ◽  
Negative Control ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Phaleria Macrocarpa ◽  
Anti Inflammatory

Objective: The plant mahkota dewa (Phaleria macrocarpa) is known to have anti-inflammatory effects. This study aimed to determine whetherchitosan nanoparticles containing mahkota dewa leaf extract would yield superior anti-inflammatory effects in the colon of a mouse model of dextransodium sulfate (DSS)-induced ulcerative colitis, compared with ethanol extract alone after testing the acute toxicities (lethal dose) of both preparations.Methods: For acute toxicity testing, 10 Sprague-Dawley rats were administered 6000 mg/kg body weight (BW) of leaf extract alone or with nanoparticles.Subsequently, mice were divided into the following six groups to determine the anti-inflammatory effects: Untreated, negative control (DSS 2% w/v), leafextract at 12.5 or 25 mg/kg BW, and leaf extract in chitosan nanoparticles at 6.25 or 12.5 mg/kg BW. To induce colitis, DSS (2% w/v) was administeredthrough drinking water for 6 weeks. The anti-inflammatory effect was observed histopathologically by imaging the inflammatory cells of the mice colonwith hematoxylin-eosin (HE) staining.Results: For acute toxicity testing, 10 Sprague-Dawley rats were administered 6000 mg/kg BW of leaf extract alone or with nanoparticles. Subsequently,mice were divided into the following six groups to determine the anti-inflammatory effects: Untreated, negative control (DSS 2% w/v), leaf extract at12.5 or 25 mg/kg BW, and leaf extract in chitosan nanoparticles at 6.25 or 12.5 mg/kg BW. To induce colitis, DSS (1% w/v) was administered throughdrinking water for 6 weeks. The anti-inflammatory effect was observed histopathologically by imaging the inflammatory cells of the mice colon withHE staining.Conclusion: Chitosan nanoparticles containing mahkota dewa leaf extract can be included in the practically non-toxic class of materials. However, anethanol extract of mahkota dewa leaf effectively inhibited DSS-induced inflammation in the mouse colon, regardless of delivery vehicle.

Magnolia officinalis Reduces Inflammation and Damage Induced by Recurrent Status Epilepticus in Immature Rats

2020 ◽  
Vol 26 (12) ◽  
pp. 1388-1401
Author(s):  
Angélica Vega-García ◽  
Luisa Rocha ◽  
Rosalinda Guevara-Guzmán ◽  
Christian Guerra-Araiza ◽  
Iris Feria-Romero ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Neuronal Loss ◽  
Preventive Treatment ◽  
Post Treatment ◽  
Sprague Dawley ◽  
Neuroprotective Effects ◽  
Sprague Dawley Rats ◽  
Immature Rats ◽  
Anti Inflammatory ◽  
Magnolia Officinalis

Background: Neuroinflammation induced in response to damage caused by status epilepticus (SE) activates the interleukin (IL)1-β pathway and proinflammatory proteins that increase vulnerability to the development of spontaneous seizure activity and/or epilepsy. Objectives: The study aimed to assess the short-term anti-inflammatory and neuroprotective effects of Magnolia officinalis (MO) on recurrent SE in immature rats. Methods: Sprague-Dawley rats at PN day 10 were used; n = 60 rats were divided into two control groups, SHAM and KA, and two experimental groups, MO (KA-MO) and Celecoxib (KA-Clbx). The anti-inflammatory effect of a single dose of MO was evaluated at 6 and 24 hr by Western blotting and on day 30 PN via a subchronic administration of MO to assess neuronal preservation and hippocampal gliosis by immunohistochemistry for NeunN and GFAP, respectively. Results: KA-MO caused a decrease in the expression of IL1-β and Cox-2 at 6 and 24 h post-treatment, a reduction in iNOS synthase at 6 and 24 hr post-treatment and reduced neuronal loss and gliosis at postnatal day 30, similar to Clbx. Conclusion: The results indicating that Magnolia officinalis is an alternative preventive treatment for early stages of epileptogenesis are encouraging.

Evaluation of Therapeutic Effects of Quercetin Against Achilles Tendinopathy in Rats via Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Metalloproteinases

2021 ◽  
pp. 036354652110598
Author(s):  
Halil Sezgin Semis ◽  
Cihan Gur ◽  
Mustafa Ileriturk ◽  
Fatih Mehmet Kandemir ◽  
Ozgur Kaynar
Keyword(s):  
Oxidative Stress ◽  
Achilles Tendinopathy ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Alternative Treatment Option ◽  
Markers Of Oxidative Stress ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
The One

Background: Achilles tendinopathy, seen in athletes and manual labor workers, is an inflammatory condition characterized by chronic tendon pain. Owing to the toxicity that develops in various organs attributed to the use of anti–inflammatory drugs, there is a need for new therapeutic agents. Purpose: In the present study, the effects of quercetin (Que), the one that attracted the most attention of researchers studying this group of flavonoids, were investigated against collagenase–induced tendinopathy. Study Design: Controlled laboratory study. Methods: A total of 35 Sprague-Dawley rats were used in the study. Tendinopathy was created by injecting a single dose of collagenase (10 μL; 10 mg/mL) into the tendons of rats. Thirty minutes after the injection, Que was administered at doses of 25 or 50 mg/kg. Que administration was carried out for 7 days. Animals underwent a motility test at the end of the study. In addition, markers of oxidative stress, inflammation, apoptosis, and autophagy, as well as the expression levels of matrix metalloproteinases (MMPs 2, 3, 9, and 13), ICAM-1, and STAT3, were measured in tendon tissues with biochemical, molecular, and Western blot techniques. Results: The results showed that oxidative stress, inflammation, apoptosis, and autophagy were triggered by the injection of collagenase. In addition, MMPs, ICAM-1, and STAT3 were activated to participate in the development of tendinopathy. Que was found to reduce ICAM-1 levels in tendon tissue. Moreover, Que showed antioxidant, anti–inflammatory, antiapoptotic, and antiautophagic effects on tendons against tendinopathy. More important, Que suppressed the expression of MMPs in the tendon tissues. Conclusion: Que has protective properties against collagenase–induced tendon damage in rats. Clinical Relevance: We believe that with further study, Que may be shown to be an alternative treatment option for athletes or others who experience tendon injuries.

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