2013
DOI: 10.2478/s13380-013-0145-y
|View full text |Cite
|
Sign up to set email alerts
|

HMGB1 suppression confers neuroprotection against stroke in diabetic rats

Abstract: Objectives: Diabetes is a principal risk factor for stroke, and results in poorer neurological outcome after stroke. High mobility group box-1 (HMGB1) was recently reported to mediate an increased inflammatory response through receptors for advanced glycation end products (RAGE) and Toll-like receptors (TLR). In this study, we investigated how blocking HMGB1, using glycyrrhizin, may reduce inflammation following ischemic stroke in a diabetic model. Methods: The effect of glycyrrhizin on non-stroke diabetic rat… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0

Year Published

2018
2018
2024
2024

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(1 citation statement)
references
References 31 publications
0
1
0
Order By: Relevance
“…HMGB-1 is a marker of cell damage, and it is released in cells during stress as danger cell signals [8,[36][37][38][39]. In response to many stresses or injuries in cells, HMGB-1 is released passively as dangerassociated molecular patterns that will trigger inflammation; thus, during acute ischemic stroke, HMGB-1 is released from neuronal cells or other cells in cerebral tissue, and this will accelerate cell injury in cerebral tissue [10,40]. During acute ischemic stroke, there is increase infree radicals as a result of oxidative stress, and this will increase HMGB-1 levels [41][42][43].…”
Section: Discussionmentioning
confidence: 99%
“…HMGB-1 is a marker of cell damage, and it is released in cells during stress as danger cell signals [8,[36][37][38][39]. In response to many stresses or injuries in cells, HMGB-1 is released passively as dangerassociated molecular patterns that will trigger inflammation; thus, during acute ischemic stroke, HMGB-1 is released from neuronal cells or other cells in cerebral tissue, and this will accelerate cell injury in cerebral tissue [10,40]. During acute ischemic stroke, there is increase infree radicals as a result of oxidative stress, and this will increase HMGB-1 levels [41][42][43].…”
Section: Discussionmentioning
confidence: 99%