Key Laboratory of Neurology of Hebei Province

Shijiazhuang, China

Key Laboratory of Neurology of Hebei Province

Shijiazhuang, China
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Ji Y.-X.,Hebei Medical University | Zhao M.,Hebei Medical University | Liu Y.-L.,Hebei Medical University | Liu Y.-L.,Key Laboratory of Neurology of Hebei Province | And 4 more authors.
Neuroscience Letters | Year: 2017

Estrogen exerts protective roles in amyotrophic lateral sclerosis (ALS). However, the expression of aromatase (ARO) and estrogen receptors (ERs) in the motoneurons of spinal cord, has not yet been elucidated. By immunohistochemistry, we found that ARO and ERs were present in the ventral horn of adult mice lumbar spinal cord, and colocalized with SMI-32, a motoneuron specific marker. Within motoneurons, we observed that ARO is detected primarily in the cytoplasm, with fewer ARO in the nucleus; ERα and ERβ mainly localized in the nucleus with less in the cytoplasm; while GPR30 is located in soma and processes. In conclusion, we found that ERs and ARO are expressed in the motoneurons of lumbar spinal cord in adult mice. These findings suggest that estrogen may be useful as a promising therapeutic agent for prevention of damage and improvement of locomotor function in ALS. © 2017 Elsevier B.V.


Chen Y.,Hebei Medical University | Chen Y.,Key Laboratory of Neurology of Hebei Province | Li B.,Key Laboratory of Neurology of Hebei Province | Li B.,Hebei Medical University | And 6 more authors.
Biochemical and Biophysical Research Communications | Year: 2015

Apolipoprotein E (ApoE) genotypes are related to clinical presentations in patients with Wilson's disease, indicating that ApoE may play an important role in the disease. However, our understanding of the role of ApoE in Wilson's disease is limited. High copper concentration in Wilson's disease induces excessive generation of free oxygen radicals. Meanwhile, ApoE proteins possess antioxidant effects. We therefore determined whether copper-induced oxidative damage differ in the liver of wild-type and ApoE knockout (ApoE-/-) mice. Both wild-type and ApoE-/- mice were intragastrically administered with 0.2 mL of copper sulfate pentahydrate (200 mg/kg; a total dose of 4 mg/d) or the same volume of saline daily for 12 weeks, respectively. Copper and oxidative stress markers in the liver tissue and in the serum were assessed. Our results showed that, compared with the wild-type mice administered with copper, TBARS as a marker of lipid peroxidation, the expression of oxygenase-1 (HO-1), NAD(P)H dehydrogenase, and quinone 1 (NQO1) significantly increased in the ApoE-/- mice administered with copper, meanwhile superoxide dismutase (SOD) activity significantly decreased. Thus, it is concluded that ApoE may protect the liver from copper-induced oxidative damage in Wilson's disease. © 2015 Elsevier Inc. All rights reserved.


PubMed | Key Laboratory of Neurology of Hebei Province, The First Hospital of Handan and Hebei Medical University
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2015

Apolipoprotein E (ApoE) genotypes are related to clinical presentations in patients with Wilsons disease, indicating that ApoE may play an important role in the disease. However, our understanding of the role of ApoE in Wilsons disease is limited. High copper concentration in Wilsons disease induces excessive generation of free oxygen radicals. Meanwhile, ApoE proteins possess antioxidant effects. We therefore determined whether copper-induced oxidative damage differ in the liver of wild-type and ApoE knockout (ApoE(-/-)) mice. Both wild-type and ApoE(-/-) mice were intragastrically administered with 0.2 mL of copper sulfate pentahydrate (200 mg/kg; a total dose of 4 mg/d) or the same volume of saline daily for 12 weeks, respectively. Copper and oxidative stress markers in the liver tissue and in the serum were assessed. Our results showed that, compared with the wild-type mice administered with copper, TBARS as a marker of lipid peroxidation, the expression of oxygenase-1 (HO-1), NAD(P)H dehydrogenase, and quinone 1 (NQO1) significantly increased in the ApoE(-/-) mice administered with copper, meanwhile superoxide dismutase (SOD) activity significantly decreased. Thus, it is concluded that ApoE may protect the liver from copper-induced oxidative damage in Wilsons disease.

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