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Mitigation Effects of a Novel Herbal Medicine Hepad, on neurophysiology.

BJ. Park, DH. Kim, JM. Park (Daejeon, Republic of Korea)

Meeting: 2019 International Congress

Abstract Number: 1779

Keywords: Neurophysiology, Parkinsonism

Session Information

Date: Wednesday, September 25, 2019

Session Title: Physiology and Pathophysiology

Session Time: 1:15pm-2:45pm

Location: Les Muses, Level 3

Objective: Therefore, further studies are needed to identify compounds that can modulate the disease process and prevent the progression of symptoms in affected patients. Our research has focused on herbal medicines for the treatment of PD.

Background: Parkinson’s disease (PD), a common adult-onset neurodegenerative disorder with complex pathological mechanisms, is characterized by the degeneration of dopaminergic nigrostriatal neurons. The molecular pathogenesis of PD is believed to be associated with mitochondrial dysfunction, oxidative stress, and activation of the apoptotic cascade. But, currently no existing drugs are capable of perfect inhibiting or delaying the progression of PD.

Method: The present study demonstrated that the herbal medicines Hepad 1 and 2 protected against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity in C57BL/6 mice and SH-SY5Y cells.

Results: Hepad 1 and 2 remarkably alleviated the enhanced expression of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase, cyclooxygenase-2, macrophage-1, and phosphorylated iκB-α) and apoptotic signals (Bcl-2-associated X protein, caspase-3, and poly [ADP-ribose] polymerase-1). Additionally, Hepad reduced MPTP-induced oxidative damage by increasing the expression of anti-oxidant defense enzymes (superoxide dismutase and glutathione S-transferase) and downregulating the levels of nicotinamide adenine dinucleotide phosphate oxidase 4. This study also showed that the neuroprotective effects of Hepad include anti-inflammatory, anti-apoptotic, and anti-oxidative properties, in addition to activation of the protein kinase B, extracellular-signal-regulated kinase, and c-Jun N-terminal kinase signaling pathways. Furthermore, oral administration of Hepad 1 and 2 attenuated the death of tyrosine hydroxylase-positive substantia nigra neurons that was induced by 20 mg/kg MPTP.

Conclusion: The present study showed for the first time that Hepad possesses anti-oxidant activity and that it can exert neuroprotective effects against MPTP-induced oxidative stress injury. Specifically, our study demonstrated that Hepad protected against MPTP-induced injury by reducing the expression of inflammatory regulators and apoptosis-associated proteins, as well as by increasing the levels of anti-oxidant enzymes via the p-AKT and MAPK signaling pathways.

To cite this abstract in AMA style:

BJ. Park, DH. Kim, JM. Park. Mitigation Effects of a Novel Herbal Medicine Hepad, on neurophysiology. [abstract]. Mov Disord. 2019; 34 (suppl 2). https://www.mdsabstracts.org/abstract/mitigation-effects-of-a-novel-herbal-medicine-hepad-on-neurophysiology/. Accessed June 14, 2025.
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