{"id":26891,"date":"2020-07-02T08:00:35","date_gmt":"2020-07-02T08:00:35","guid":{"rendered":"https:\/\/wames.org.uk\/cms-english\/?p=26891"},"modified":"2020-07-02T08:02:12","modified_gmt":"2020-07-02T08:02:12","slug":"26891-2","status":"publish","type":"post","link":"https:\/\/wames.org.uk\/cms-english\/26891-2\/","title":{"rendered":"Protective effect of hemin against experimental CFS in mice: possible role of neurotransmitters"},"content":{"rendered":"

Protective effect of hemin against experimental Chronic Fatigue Syndrome in mice: possible role of neurotransmitters<\/a>, by Vandana Thakur, Sumit Jamwal, Mandeep Kumar, Vikrant Rahi & Puneet Kumar\u00a0 in<\/span> Neurotoxicity Research<\/em> (2020) [doi.org\/10.1007\/s12640-020-00231-y]<\/h3>\n

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Research abstract:<\/strong><\/h3>\n

Chronic fatigue syndrome (CFS) is a disorder characterized by persistent and relapsing fatigue along with long-lasting and debilitating fatigue, myalgia, cognitive impairment, and many other common symptoms.<\/p>\n

The present study was conducted to explore the protective effect of hemin<\/a> on CFS in experimental mice. Male albino mice were subjected to stress-induced CFS in a forced swimming test apparatus for 21\u00a0days. After animals had been subjected to the forced swimming test, hemin (5 and 10\u00a0mg\/kg; i.p.) and hemin (10\u00a0mg\/kg) + tin(IV) protoporphyrin (SnPP), a hemeoxygenase-1 (HO-1) enzyme inhibitor, were administered daily for 21\u00a0days.<\/p>\n

Various behavioral tests (immobility period, locomotor activity, grip strength, and anxiety) and estimations of biochemical parameters (lipid peroxidation<\/a>, nitrite<\/a>, and GSH<\/a>), mitochondrial complex dysfunctions<\/a> (complexes I and II), and neurotransmitters<\/a> (dopamine, serotonin, and norepinephrine and their metabolites) were subsequently assessed.<\/p>\n

Animals exposed to 10\u00a0min of forced swimming session for 21\u00a0days showed a fatigue-like behavior (as increase in immobility period, decreased grip strength, and anxiety) and biochemical alteration observed by increased oxidative stress, mitochondrial dysfunction, and neurotransmitter level alteration.<\/p>\n

\"\"Treatment with hemin (5 and 10\u00a0mg\/kg) for 21\u00a0days significantly improved the decreased immobility period, increased locomotor activity, and improved anxiety-like behavior, oxidative defense, mitochondrial complex dysfunction, and neurotransmitter level in the brain.<\/p>\n

Further, these observations were reversed by SnPP<\/a>, suggesting that the antifatigue effect of hemin is HO-1 dependent. The present study highlights the protective role of hemin against experimental CFS-induced behavioral, biochemical, and neurotransmitter alterations.<\/p>\n

Read full article<\/a><\/p>\n

ME Research UK<\/strong>: Hemin protects against CFS-like symptoms in mice<\/a><\/p>\n

Key findings<\/strong><\/p>\n