خواص قارچ ها, دانستنی ها, مقالات علمی

تاثیر قارچ گانودرما روی بیماری پارکینسون

مقاله 2018: یافته های جدید در ارتباط با تاثیر قارچ گانودرما/گنودرما روی بیماری پارکینسون
مطالعات اخیر نشان داده است که این قارچ از تخریب سلول های عصبی محافظت می کند. در این مقاله مکانیسم این عمل تشریح می شود. به طور خلاصه، نتایج این تحقیق نشان می دهد که گانودرما باعث کاهش پارکینسون از طریق تنظیم عملکرد میتوکندری، اتوفاژی و آپوپتوزیز است. این فرایند شامل فعال شدن هر دو مسیر سیگنالینگ AMPK / mTOR و PINK1 / Parkin است.

برای مطالعه مطلب ده دلیل برای اینکه گانودرما داروی جاودانگی است کلیک کنید

Acta Pharmacol Sin. 2018
Ganoderma lucidum extract ameliorates MPTP-induced parkinsonism and protects dopaminergic neurons from oxidative stress via regulating mitochondrial function, autophagy, and apoptosis.
Abstract
Neuroprotection targeting mitochondrial dysfunction has been proposed as an important therapeutic strategy for Parkinson’s disease. Ganoderma lucidum (GL) has emerged as a novel agent that protects neurons from oxidative stress. However, the detailed mechanisms underlying GL-induced neuroprotection have not been documented. In this study, we investigated the neuroprotective effects of GL extract (GLE) and the underlying mechanisms in the classic MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-induced mouse model of PD. Mice were injected with MPTP to induce parkinsonism. Then the mice were administered GLE (400 mg kg-1 d-1, ig) for 4 weeks. We observed that GLE administration significantly improved locomotor performance and increased tyrosine hydroxylase expression in the substantia nigra pars compact (SNpc) of MPTP-treated mice. In in vitro study, treatment of neuroblastoma neuro-2a cells with 1-methyl-4-phenylpyridinium (MPP+, 1 mmol/L) caused mitochondrial membrane potential collapse, radical oxygen species accumulation, and ATP depletion. Application of GLE (800 μg/mL) protected neuroblastoma neuro-2a cells against MPP+ insult. Application of GLE also improved mitochondrial movement dysfunction in cultured primary mesencephalic neurons. In addition, GLE counteracted the decline in NIX (also called BNIP3L) expression and increase in the LC3-II/LC3-I ratio evoked by MPP+. Moreover, GLE reactivated MPP+-inhibited AMPK, mTOR, and ULK1. Similarly, GLE was sufficient to counteract MPP+-induced inhibition of PINK1 and Parkin expression. GLE suppressed MPP+-induced cytochrome C release and activation of caspase-3 and caspase-9. In summary, our results provide evidence that GLE ameliorates parkinsonism pathology via regulating mitochondrial function, autophagy, and apoptosis, which may involve the activation of both the
AMPK/mTOR and PINK1/Parkin signaling pathway

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https://www.ncbi.nlm.nih.gov/pubmed/29991712

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