4.7 Review

Potential therapeutic effects and pharmacological evidence of sinomenine in central nervous system disorders

Journal

FRONTIERS IN PHARMACOLOGY
Volume 13, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2022.1015035

Keywords

sinomenine; oxidative stress; neuroinflammation; autophagy; apoptosis

Funding

  1. Science and Technology Project of Nantong City [JC2020013, JC2020020]
  2. Natural Science Foundation of Jiangsu Province [BK20221375]
  3. Postgraduate Research and Practice Innovation Program of Jiangsu Province [KYCX21_3107]
  4. Natural Science Foundation of the Higher Education Institutions of Jiangsu Province [20KJB310025]

Ask authors/readers for more resources

Sinomenine, a natural compound from Sinomenium acutum, has shown beneficial effects in various CNS disorders, including cerebral ischemia, traumatic brain injury, Alzheimer's disease, Parkinson's disease, and epilepsy. Its mechanisms of action involve inhibition of oxidative stress, neuroinflammation, and neuronal apoptosis. Sinomenine also exhibits anti-glioma effects and improves morphine dependence and sleep disturbance.
Sinomenine is a natural compound extracted from the medicinal plant Sinomenium acutum. Its supplementation has been shown to present benefits in a variety of animal models of central nervous system (CNS) disorders, such as cerebral ischemia, intracerebral hemorrhage, traumatic brain injury (TBI), Alzheimer's disease (AD), Parkinson's disease (PD), epilepsy, depression, multiple sclerosis, morphine tolerance, and glioma. Therefore, sinomenine is now considered a potential agent for the prevention and/or treatment of CNS disorders. Mechanistic studies have shown that inhibition of oxidative stress, microglia- or astrocyte-mediated neuroinflammation, and neuronal apoptosis are common mechanisms for the neuroprotective effects of sinomenine. Other mechanisms, including activation of nuclear factor E2-related factor 2 (Nrf2), induction of autophagy in response to inhibition of protein kinase B (Akt)-mammalian target of rapamycin (mTOR), and activation of cyclic adenosine monophosphate-response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF), may also mediate the anti-glioma and neuroprotective effects of sinomenine. Sinomenine treatment has also been shown to enhance dopamine receptor D2 (DRD2)mediated nuclear translocation of aB-crystallin (CRYAB) in astrocytes, thereby suppressing neuroinflammation via inhibition of Signal Transducer and Activator of Transcription 3 (STAT3). In addition, sinomenine supplementation can suppress N-methyl-D-aspartate (NMDA) receptormediated Ca2+ influx and induce.-aminobutyric acid type A (GABAA) receptor-mediated Cl- influx, each of which contributes to the improvement of morphine dependence and sleep disturbance. In this review, we outline the pharmacological effects and possible mechanisms of sinomenine in CNS disorders to advance the development of sinomenine as a new drug for the treatment of CNS disorders.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available