Mitochondrial Dysfunction Meets its Match: Huangqin Decoction Shows Promise in Treating Parkinson’s Disease

Published on July 15, 2022

Imagine a ship sailing smoothly through calm waters, its engine running at peak performance. Now, envision a ship struggling against rough seas, its engine faltering and sputtering. Just like a ship relies on its engine for smooth sailing, our brain cells depend on mitochondria for optimal function. In Parkinson’s Disease (PD), these mitochondria go awry, leading to the deterioration of brain cells. However, a recent study has found that Huangqin Decoction (HQD), a traditional Chinese medicine, may hold the key to combating mitochondrial dysfunction in PD. By improving motor coordination, muscle strength, and the number of neurons, HQD appears to shield against the effects of PD. Additionally, HQD enhances mitochondrial function by increasing ATP production and mitochondrial complex I activity. Interestingly, the study also discovered elevated levels of ketone bodies – alternative energy sources for the brain – in PD rats. Furthermore, HQD boosted glucose metabolism and suppressed ketone body production and transport. This groundbreaking research sheds light on the potential of HQD as a therapeutic tool in treating PD by activating the aerobic glycolysis pathway. So hop aboard this exciting scientific journey and dive into the details of this study!

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 β-hydroxybutyric acid (β-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.

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