Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease
Parkinson’s disease (PD) is regarded as a severe neurodegenerative disorder. Baicalein is involved in the treatment of PD. This study explored the mechanism of baicalein in PD. The PD rat model was established using 6-hydroxydopamine. The neurologic score, dopamine (DA) content, apoptotic cells, and...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Biochemistry Research International |
| Online Access: | http://dx.doi.org/10.1155/2021/2319412 |
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| author | Min Chen Li Peng Ping Gong Xiaoli Zheng Tao Sun Xiaoqiao Zhang Jiangtao Huo |
| author_facet | Min Chen Li Peng Ping Gong Xiaoli Zheng Tao Sun Xiaoqiao Zhang Jiangtao Huo |
| author_sort | Min Chen |
| collection | DOAJ |
| description | Parkinson’s disease (PD) is regarded as a severe neurodegenerative disorder. Baicalein is involved in the treatment of PD. This study explored the mechanism of baicalein in PD. The PD rat model was established using 6-hydroxydopamine. The neurologic score, dopamine (DA) content, apoptotic cells, and neuronal damage were evaluated after rats were treated with baicalein. Autophagy in PD rats was inhibited using 3-methyladenine (3-MA). The mitochondrial membrane potential (MMP) and autophagy-related proteins (LC3, P62) were detected. Next, agomiR-30b was transfected into PD rats. The targeting relation between miR-30b and NIX was predicted and verified. Then, sh-NIX was transfected into PD rats, and the effects of miR-30b and NIX on MMP, LC3, and P62 were assessed. When miR-30b was overexpressed using agomiR-30b, the NIX and BNIP3 levels were detected. Baicalein increased the neurological score and restored DA content, neurons, MMP, and mitochondrial autophagy protein levels. Baicalein inhibited miR-30b expression and miR-30b targeted NIX. miR-30b upregulation or NIX silencing reversed the effect of baicalein on MMP and mitochondrial autophagy. Baicalein upregulated NIX and BNIP3 expressions, while miR-30b overexpression inhibited NIX and BNIP3 expressions. In summary, baicalein mediated mitochondrial autophagy and restored neuronal activity by downregulating miR-30b and activating the NIX/BNIP3 pathway, thus protecting against PD. |
| format | Article |
| id | doaj-art-7c7cc8d4844945dfa4ddb546f0273341 |
| institution | OA Journals |
| issn | 2090-2247 2090-2255 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Biochemistry Research International |
| spelling | doaj-art-7c7cc8d4844945dfa4ddb546f02733412025-08-20T02:07:24ZengWileyBiochemistry Research International2090-22472090-22552021-01-01202110.1155/2021/23194122319412Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s DiseaseMin Chen0Li Peng1Ping Gong2Xiaoli Zheng3Tao Sun4Xiaoqiao Zhang5Jiangtao Huo6Department of Geriatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, ChinaDepartment of Geriatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, ChinaDepartment of Geriatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, ChinaDepartment of Geriatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, ChinaDepartment of Surgery, Traditional Chinese Medicine Hospital of Qiandongnan Miao and Dong Autonomous Prefecture, Kaili 556000, Guizhou, ChinaDepartment of Geriatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, ChinaDepartment of Geriatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, ChinaParkinson’s disease (PD) is regarded as a severe neurodegenerative disorder. Baicalein is involved in the treatment of PD. This study explored the mechanism of baicalein in PD. The PD rat model was established using 6-hydroxydopamine. The neurologic score, dopamine (DA) content, apoptotic cells, and neuronal damage were evaluated after rats were treated with baicalein. Autophagy in PD rats was inhibited using 3-methyladenine (3-MA). The mitochondrial membrane potential (MMP) and autophagy-related proteins (LC3, P62) were detected. Next, agomiR-30b was transfected into PD rats. The targeting relation between miR-30b and NIX was predicted and verified. Then, sh-NIX was transfected into PD rats, and the effects of miR-30b and NIX on MMP, LC3, and P62 were assessed. When miR-30b was overexpressed using agomiR-30b, the NIX and BNIP3 levels were detected. Baicalein increased the neurological score and restored DA content, neurons, MMP, and mitochondrial autophagy protein levels. Baicalein inhibited miR-30b expression and miR-30b targeted NIX. miR-30b upregulation or NIX silencing reversed the effect of baicalein on MMP and mitochondrial autophagy. Baicalein upregulated NIX and BNIP3 expressions, while miR-30b overexpression inhibited NIX and BNIP3 expressions. In summary, baicalein mediated mitochondrial autophagy and restored neuronal activity by downregulating miR-30b and activating the NIX/BNIP3 pathway, thus protecting against PD.http://dx.doi.org/10.1155/2021/2319412 |
| spellingShingle | Min Chen Li Peng Ping Gong Xiaoli Zheng Tao Sun Xiaoqiao Zhang Jiangtao Huo Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease Biochemistry Research International |
| title | Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease |
| title_full | Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease |
| title_fullStr | Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease |
| title_full_unstemmed | Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease |
| title_short | Baicalein Mediates Mitochondrial Autophagy via miR-30b and the NIX/BNIP3 Signaling Pathway in Parkinson’s Disease |
| title_sort | baicalein mediates mitochondrial autophagy via mir 30b and the nix bnip3 signaling pathway in parkinson s disease |
| url | http://dx.doi.org/10.1155/2021/2319412 |
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