Abstract
Few pharmaceutical agents for slowing Parkinson's disease (PD) progression existed, especially for perimenopause females. The current general medications are mostly hormone replacement therapy and may have some side effects. Therefore, there is an urgent need for a novel treatment for PD. This study examined the possibility of estradiol plus lithium chloride (LiCl), one of the metal halides used as an alternative to salt. We showed that the combination of LiCl and estradiol could enhance neurogenesis proteins GAP-43 and N-myc in the human neuronal-like cells. We also further confirmed the neurogenesis activity in zebrafish. LiCl and LiCl plus estradiol could enhance 6-OHDA-induced upregulation of TGase-2b and Rho A mRNA expression. Besides, LiCl plus estradiol showed a synergic effect in anti-apoptotic activity. LiCl plus estradiol protected SH-SY5Y cells and zebrafish against 6-OHDA-induced damage on neurons than LiCl or estradiol alone groups via p-P38, p-Akt, Bcl-2, and caspase-3 cascade. The potential for developing this combination as a candidate treatment for PD is discussed.
Highlights
Parkinson’s disease (PD) is one of the most complex neurodegenerative diseases in the world
We firstly examined the neuroprotective effect of the combination of lithium chloride and estradiol (E2) on the SHSY5Y neuroblastoma cell line. e following tests evaluated the anti-apoptotic activity, including cell viability, TUNEL staining, cleavage caspase-3 mRNA, and protein expression
Our result demonstrated that 1 mΜ LiCl plus 100 nM E2 significantly attenuated 6-OHDAinduced upregulation of cleaved caspase-3 mRNA expression (566.2 ± 33.5% to 222.5 ± 10.2%) (Figure 2(b)). e protein expression was consistent with mRNA expression. e co-treatment of 1 mΜ LiCl plus 100 nM E2 significantly attenuated 6-OHDA-induced upregulation of cleaved caspase-3 protein expression (133.4 ± 5.4% to 70.3 ± 10.3%) (Figure 2(c))
Summary
Parkinson’s disease (PD) is one of the most complex neurodegenerative diseases in the world. Picillo et al demonstrated that perimenopause might increase the possibility of developing a neurodegenerative disease in female patients [1]. Hormone therapy has become a choice in perimenopause patients. E first study that revealed the neuroprotective role of estrogen came from Hall et al is study examined the therapeutic efficacy of estrogen in different gender of traumatic brain injury models, and the result showed that female gerbils suffered less than male gerbils [2]. Some further studies used exogenous estrogen to inhibit the volume of thrombosis in the ischemia rat model [3, 4]. Gibson et al systemically reviewed 161 original articles, including 1304 individuals, and revealed that estrogen had a significant therapeutic effect in neurodegenerative animal models [5]. En, hormone replacement therapy (HRT) began to be used in patients Gibson et al systemically reviewed 161 original articles, including 1304 individuals, and revealed that estrogen had a significant therapeutic effect in neurodegenerative animal models [5]. en, hormone replacement therapy (HRT) began to be used in patients
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