Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

987
Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
987
Neural Regulation01:37

Neural Regulation

43.1K
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
43.1K
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

1.8K
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
1.8K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

9.8K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
9.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Efficacy of anastomotic reinforcement suture in laparoscopic anterior resection for middle-low rectal cancer: a propensity-score-matched cohort study.

BMC surgery·2026
Same author

Chloroplast sunscreening by protein condensates confers high-light tolerance.

Cell·2026
Same author

Training climate matters: programmatic openness, individual belonging, and trainee mistreatment in graduate medical education.

Medical education online·2026
Same author

A Computer Numerical Control Wire Electrical Discharge Machining Strategy for Fabricating Cobalt-Copper Bimetallic Oxide Maze-like Micro-Supercapacitors.

Micromachines·2026
Same author

Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).

Molecular medicine reports·2026
Same author

Choose Your Own Adventure! A Novel Approach in Ethics Teaching.

The clinical teacher·2026

Related Experiment Video

Updated: Jan 17, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
15:09

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Published on: October 3, 2012

17.3K

Sinomenine Modifies Parkinson's Disease Through Nrf2 Activation.

Lingling Zhu1, Lin Lin1,2, Zhenyu Yang3

  • 1Department of Pharmacy, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, No.150, Ximen Street, Linhai, 317000, Zhejiang Province, China.

Neurochemical Research
|September 18, 2025
PubMed
Summary

Sinomenine shows potential as a Parkinson's disease therapy by activating the Nrf2/ARE pathway. This treatment reduces oxidative stress and neuroinflammation in cellular and animal models, improving motor function and protecting dopaminergic neurons.

Keywords:
Disease-modifyingNrf2/ARENuclear translocationParkinson’s diseaseSinomenine

More Related Videos

Cell Based Assays of SINEUP Non-coding RNAs That Can Specifically Enhance mRNA Translation
10:21

Cell Based Assays of SINEUP Non-coding RNAs That Can Specifically Enhance mRNA Translation

Published on: February 1, 2019

8.7K

Related Experiment Videos

Last Updated: Jan 17, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
15:09

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Published on: October 3, 2012

17.3K
Cell Based Assays of SINEUP Non-coding RNAs That Can Specifically Enhance mRNA Translation
10:21

Cell Based Assays of SINEUP Non-coding RNAs That Can Specifically Enhance mRNA Translation

Published on: February 1, 2019

8.7K

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Parkinson's disease (PD) lacks disease-modifying treatments.
  • The Nrf2/ARE pathway is a promising therapeutic target for PD.
  • Sinomenine's effects on PD and Nrf2/ARE activation require investigation.

Purpose of the Study:

  • To investigate the therapeutic potential of sinomenine in Parkinson's disease.
  • To explore the role of sinomenine in activating the Nrf2/ARE pathway.
  • To evaluate sinomenine's effects on oxidative stress, inflammation, and neuronal survival in PD models.

Main Methods:

  • Utilized 6-OHDA-induced Parkinsonian cell (SH-SY5Y) and rat models.
  • Assessed cell viability, apoptosis, and reactive oxygen species (ROS) levels.
  • Measured Nrf2 pathway activation, antioxidant enzyme expression, and neuroinflammation markers (TNF-α, IL-1β).
  • Evaluated behavioral changes, dopaminergic neuron survival, and striatal tyrosine hydroxylase (TH) levels in vivo.
  • Confirmed Nrf2 nuclear translocation and performed molecular docking with Keap1.

Main Results:

  • Sinomenine treatment reduced apoptosis and ROS, enhancing cell viability in vitro.
  • Nrf2 silencing abolished the protective effects of sinomenine, confirming Nrf2 dependence.
  • In vivo, sinomenine improved motor function, increased TH levels, and preserved dopaminergic neurons.
  • Sinomenine suppressed neuroinflammation by reducing TNF-α and IL-1β and normalizing microglial morphology.
  • Molecular docking indicated high affinity between sinomenine and Keap1, promoting Nrf2 nuclear translocation.

Conclusions:

  • Sinomenine activates the Nrf2/ARE pathway, offering protection against oxidative stress and neuroinflammation in PD models.
  • The mechanism involves Keap1 binding, leading to Nrf2 nuclear translocation.
  • Sinomenine demonstrates potential as a disease-modifying therapy for Parkinson's disease.