CYBERMED LIFE - ORGANIC  & NATURAL LIVING

Thymoquinone

  • Reduction of side effects of hyperbaric oxygen therapy with thymoquinone treatment in rats.

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    Abstract Title:

    Reduction of side effects of hyperbaric oxygen therapy with thymoquinone treatment in rats.

    Abstract Source:

    Undersea Hyperb Med. 2017 Jul-Aug;44(4):337-343. PMID: 28783890

    Abstract Author(s):

    Ali Erdal Gunes, Orhan Gozeneli, Muhammed Emin Guldur

    Article Affiliation:

    Ali Erdal Gunes

    Abstract:

    INTRODUCTION:Hyperbaric oxygen (HBO₂) treatment results in elevated production of reactive oxygen species (ROS) that leads to cellular damage. Thymoquinone (TQ) is reported to have anti-inflammatory and antimicrobial activity and may suppress the generation of free radicals. The goal of this study is reduction of side effects of hyperbaric oxygen therapy with thymoquinone treatment.

    METHODS:30 female Sprague-Dawley rats were randomly assigned to one of three groups (n = 10 per group). Group 1 represented the control group (no treatment). Group 2 was exposed to 100% oxygen at 2.5 ATA for two sessions of two hours'duration each day for five days. Group 3 was treated identically to Group 2 and was also given thymoquinone once daily at 50 mg/kg/day by oral gavage for five days, after first session of HBO₂.

    RESULTS:LOOH and SH levels were significantly elevated in the group receiving HBO₂ treatment relative to the control group rats. Fetuin A is increased during TQ treatment. LOOH and SH levels were significantly decreased in animals treated with TQ.

    CONCLUSIONS:Long-term and repeated HBO₂ treatment leads to damage to the lung tissue. In urgent situations or cases of severe hypoxia, repeated HBO₂ sessions may be necessary, and TQ antioxidant agents may be useful for prevention of HBO₂-associated injury. TQ may represent a useful therapeutic option during HBO₂ treatment.

  • Thymoquinone loaded solid lipid nanoparticles counteracts 3-Nitropropionic acid induced motor impairments and neuroinflammation in rat model of Huntington's disease.

    Abstract Title:

    Thymoquinone loaded solid lipid nanoparticles counteracts 3-Nitropropionic acid induced motor impairments and neuroinflammation in rat model of Huntington's disease.

    Abstract Source:

    Metab Brain Dis. 2018 Oct ;33(5):1459-1470. Epub 2018 May 31. PMID: 29855977

    Abstract Author(s):

    Surekha Ramachandran, Sumathi Thangarajan

    Article Affiliation:

    Surekha Ramachandran

    Abstract:

    Defect in gene transcription, excitotoxicity, neuroinflammation and oxidative stress are the dominant disease process that causes striatal cell loss with motor abnormalities in Huntington's disease (HD). Homogeneous pathological reminiscent of HD was extrapolated in the present study using a potent mitochondrial toxin, 3-Nitropropionic acid (3-NP). Administration of 3-NP for 14 days in the present study portends glial cell activation, N-methyl-D-aspartate (NMDA) receptor stimulation, neuroinflammation and motor deficits. The therapeutic strategy in the present study was improvised by formulating thymoquinone, a biologically active compound into a colloidal carrier namelysolid lipid nanoparticles. Treatment with 10 and 20 mg/kg b.w of thymoquinone loaded solid lipid nanoparticles (TQ-SLNs) and 80 mg/kg b.w of thymoquinone suspension (TQ-S) showed a significant (P < 0.01) improvement in ATPases function in 3-NP induced animals than TQ-S (40 mg/kg b.w) treated group. TQ-SLNs (10 and 20 mg/kg) treatment also attenuated the overexpression of glial fibrillary acidic protein (GFAP), pro-inflammatory cytokines and p-p65 NFκB nuclear translocation in 3-NP exposed animals. Further, TQ-SLNs treatment desensitizes NR2B-subtype NMDA receptor, improves tyrosine hydroxylase (TH) immune reactive neurons and ameliorated the motor abnormalities in 3-NP intoxicated animals than TQ-S treated group. Hence, the study signifies that the treatment with lower doses of nanoformulated thymoquinone than thymoquinone suspension can efficiently culminate 3-NP induced HD progression in the striatum of male wistar rats.

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