Di-Huang-Yi-Zhi herbal formula attenuates amyloid-β-induced neurotoxicity in PC12 cells

An,Hong‑Mei; Lin,Chen; Gu,Chao; Chen,Jin‑Jun; Sun,Wen‑Xian; Jin,Miao; Zhang,Tian‑Li; Qiu,Ming‑Feng; Hu,Bing

doi:10.3892/etm.2017.4368

Di-Huang-Yi-Zhi herbal formula attenuates amyloid-β-induced neurotoxicity in PC12 cells

Authors:
- Hong‑Mei An
- Chen Lin
- Chao Gu
- Jin‑Jun Chen
- Wen‑Xian Sun
- Miao Jin
- Tian‑Li Zhang
- Ming‑Feng Qiu
- Bing Hu
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Affiliations: Department of Neurology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China, Department of Plastic and Reconstructive Surgery, Shanghai Key Laboratory of Tissue Engineering, The Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200011, P.R. China, School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, P.R. China, Department of Oncology and Institute of Traditional Chinese Medicine in Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R. China
Published online on: April 20, 2017 https://doi.org/10.3892/etm.2017.4368
Pages: 3003-3008

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Abstract

Traditional Chinese medicine can be used for Alzheimer's disease management, such as the modern herbal formula Di-Huang-Yi-Zhi (DHYZ). In the present study, neuronal differentiated PC12 cells were used as a model to evaluate the effects of DHYZ against amyloid‑β peptide 25‑35 (Aβ25‑35) induced neurotoxicity, particularly regarding cell proliferation, apoptosis and related events. Following treatment with DHYZ, cell viability, cell membrane damage, apoptosis, mitochondrial membrane potential, cytochrome c release, caspase‑3 activity and levels of reactive oxygen species in PC12 cells were detected. The results demonstrated that pretreatment with DHYZ significantly protected PC12 cells from Aβ25‑35‑induced proliferation inhibition, lactate dehydrogenase release and apoptosis, as well as upregulating mitochondrial membrane potential and downregulating cytochrome c release and caspase‑3 activation. DHYZ also inhibited the Aβ25‑35‑induced reactive oxygen species generation in PC12 cells. These observations suggest that DHYZ protected PC12 cells from the Aβ-induced neurotoxicity.