ArticleNeuropsychiatric disease and treatment2015
Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway.
Article in Neuropsychiatric disease and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- The therapeutic potential of triptolide and celastrol in neurological diseases.Frontiers in pharmacology · 2022Review
- The Current Status of Neuroprotection in Congenital Heart Disease.Children (Basel, Switzerland) · 2021Review
- Article
- Effectiveness of arginase inhibitors against experimentally induced stroke.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Triptolide reduces ischemia/reperfusion injury in rats and H9C2 cells via inhibition of NF‑κB, ROS and the ERK1/2 pathway.International journal of molecular medicine · 2018Article
- Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway.Experimental and therapeutic medicine · 2017Article
- Neuroprotection by triptolide against cerebral ischemia/reperfusion injury through the inhibition of NF-κB/PUMA signal in rats.Therapeutics and clinical risk management · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
Inflammation plays critical roles in the acute progression of the pathology of ischemic injury. Previous studies have shown that triptolide interferes with a number of pro-inflammatory mechanisms. In this study, we investigated whether triptolide has protective effects during acute cerebral ischemia/reperfusion (I/R) injury. Male Sprague Dawley rats received triptolide or vehicle at the onset of reperfusion following middle cerebral artery occlusion. Twenty-four hours after reperfusion, we evaluated neurological injuries, the expression of pro-inflammatory markers, and NF-κB activation. I/R rats treated with triptolide showed significantly better neurological deficit scores, decreased neural apoptosis, and reduced cerebral infarct volume and brain edema, and triptolide treatment suppressed the activation of NF-κB following I/R injury. Furthermore, the expression levels of pro-inflammatory cytokines at both the mRNA and protein levels were significantly decreased in rats receiving triptolide. These results indicate that the neuroprotective effects of triptolide during acute cerebral I/R injury are possibly related to the inhibition of both the NF-κB signaling pathway and inflammation.
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