PMID- 35912075 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20220802 IS - 1663-4365 (Print) IS - 1663-4365 (Electronic) IS - 1663-4365 (Linking) VI - 14 DP - 2022 TI - Huangqin Decoction Exerts Beneficial Effects on Rotenone-Induced Rat Model of Parkinson's Disease by Improving Mitochondrial Dysfunction and Alleviating Metabolic Abnormality of Mitochondria. PG - 911924 LID - 10.3389/fnagi.2022.911924 [doi] LID - 911924 AB - Parkinson's disease (PD) is a common neurodegenerative disease, and the pathogenesis of PD is closely related to mitochondrial dysfunction. Previous studies have indicated that traditional Chinese medicine composition of Huangqin Decoction (HQD), including Scutellariae Radix, licorice, and Paeoniae Radix Alba, has therapeutic effects on PD, but whether HQD has a therapeutic effect on PD has not been reported. In this study, the protective effects of HQD on rotenone-induced PD rats were evaluated by behavioral assays (open field, rotating rod, suspension, gait, inclined plate, and grid) and immunohistochemistry. The mechanisms of HQD on attenuation of mitochondrial dysfunction were detected by biochemical assays and mitochondrial metabolomics. The results showed that HQD (20 g/kg) can protect rats with PD by improving motor coordination and muscle strength, increasing the number of tyrosine hydroxylase (TH)-positive neurons in rats with PD. Besides, HQD can improve mitochondrial dysfunction by increasing the content of adenosine triphosphate (ATP) and mitochondrial complex I. Mitochondrial metabolomics analysis revealed that the ketone body of acetoacetic acid (AcAc) in the rotenone group was significantly higher than that of the control group. Ketone bodies have been known to be used as an alternative energy source to provide energy to the brain when glucose was deficient. Further studies demonstrated that HQD could increase the expression of glucose transporter GLUT1, the content of tricarboxylic acid cycle rate-limiting enzyme citrate synthase (CS), and the level of hexokinase (HK) in rats with PD but could decrease the content of ketone bodies [AcAc and beta-hydroxybutyric acid (beta-HB)] and the expression of their transporters (MCT1). Our study revealed that the decrease of glucose metabolism in the rotenone group was parallel to the increase of substitute substrates (ketone bodies) and related transporters, and HQD could improve PD symptoms by activating the aerobic glycolysis pathway. CI - Copyright (c) 2022 Gao, Cao, Du and Qin. FAU - Gao, Li AU - Gao L AD - Modern Research Center for Traditional Chinese Medicine, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China. AD - Key Laboratory of Effective Substances Research and Utilization in TCM of Shanxi Province, Taiyuan, China. FAU - Cao, Min AU - Cao M AD - Modern Research Center for Traditional Chinese Medicine, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China. AD - Key Laboratory of Effective Substances Research and Utilization in TCM of Shanxi Province, Taiyuan, China. FAU - Du, Guan-Hua AU - Du GH AD - Peking Union Medical College, Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, China. FAU - Qin, Xue-Mei AU - Qin XM AD - Modern Research Center for Traditional Chinese Medicine, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China. AD - Key Laboratory of Effective Substances Research and Utilization in TCM of Shanxi Province, Taiyuan, China. LA - eng PT - Journal Article DEP - 20220715 PL - Switzerland TA - Front Aging Neurosci JT - Frontiers in aging neuroscience JID - 101525824 PMC - PMC9334858 OTO - NOTNLM OT - Huangqin Decoction OT - Parkinson's disease OT - aerobic glycolysis OT - ketone bodies OT - mitochondria COIS- The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. EDAT- 2022/08/02 06:00 MHDA- 2022/08/02 06:01 PMCR- 2022/01/01 CRDT- 2022/08/01 03:56 PHST- 2022/04/03 00:00 [received] PHST- 2022/06/20 00:00 [accepted] PHST- 2022/08/01 03:56 [entrez] PHST- 2022/08/02 06:00 [pubmed] PHST- 2022/08/02 06:01 [medline] PHST- 2022/01/01 00:00 [pmc-release] AID - 10.3389/fnagi.2022.911924 [doi] PST - epublish SO - Front Aging Neurosci. 2022 Jul 15;14:911924. doi: 10.3389/fnagi.2022.911924. eCollection 2022.