PMID- 23414442
OWN - NLM
STAT- MEDLINE
DCOM- 20131022
LR  - 20231213
IS  - 1742-2094 (Electronic)
IS  - 1742-2094 (Linking)
VI  - 10
DP  - 2013 Feb 17
TI  - Rosmarinic acid protects against experimental diabetes with cerebral ischemia: 
      relation to inflammation response.
PG  - 28
LID - 10.1186/1742-2094-10-28 [doi]
AB  - BACKGROUND: Inflammatory activation plays a vital role in the pathophysiological 
      mechanisms of stroke, exerting deleterious effects on the progression of tissue 
      damage and may lead to the vascular damage in diabetes. The objectives of this 
      study were to determine the effects of rosmarinic acid (RA) on a cultured 
      neuronal cell line, SH-SY5Y in vitro and experimental ischemic diabetic stroke in 
      vivo. METHODS: For oxygen-glucose deprivation (OGD) and tumor necrosis factor-alpha 
      (TNF-alpha) stimulated SH-SY5Y cell line in vitro, SH-SY5Y cells were incubated with 
      RA. For an in vivo experiment, diabetic rats were subjected to middle cerebral 
      artery occlusion (MACO) for 40 minutes followed by reperfusion for 23 h. RESULTS: 
      Treatment of SH-SY5Y cells with RA reduced the OGD-induced apoptosis and 
      cytotoxicity, blocked TNF-alpha-induced nuclear transcription factor kappaB (NF-kappaB) 
      activation, and decreased high-mobility group box1 (HMGB1) expression. At doses 
      higher than 50 mg/kg, RA produced a significant neuroprotective potential in rats 
      with ischemia and reperfusion (I/R). RA (50 mg/kg) demonstrated significant 
      neuroprotective activity even after delayed administration at 1 h, 3 h and 5 h 
      after I/R. RA 50 mg/kg attenuated histopathological damage, decreased brain 
      edema, inhibited NF-kappaB activation and reduced HMGB1 expression. CONCLUSION: These 
      data show that RA protects the brain against I/R injury with a favorable 
      therapeutic time-window by alleviating diabetic cerebral I/R injury and 
      attenuating blood-brain barrier (BBB) breakdown, and its protective effects may 
      involve HMGB1 and the NF-kappaB signaling pathway.
FAU - Luan, Haiyun
AU  - Luan H
AD  - School of Pharmaceutical Sciences and Institute of Material Medica, Binzhou 
      Medical University, Yantai 264003, People's Republic of China.
FAU - Kan, Zechun
AU  - Kan Z
FAU - Xu, Yong
AU  - Xu Y
FAU - Lv, Changjun
AU  - Lv C
FAU - Jiang, Wanglin
AU  - Jiang W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130217
PL  - England
TA  - J Neuroinflammation
JT  - Journal of neuroinflammation
JID - 101222974
RN  - 0 (Cinnamates)
RN  - 0 (Depsides)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Neuroprotective Agents)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/metabolism/*prevention & control
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects/physiology
MH  - Cinnamates/pharmacology/*therapeutic use
MH  - Depsides/pharmacology/*therapeutic use
MH  - Diabetes Mellitus, Experimental/metabolism/*prevention & control
MH  - Humans
MH  - Inflammation Mediators/antagonists & inhibitors/*metabolism
MH  - Male
MH  - Neuroprotective Agents/pharmacology/*therapeutic use
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Rosmarinic Acid
PMC - PMC3614882
EDAT- 2013/02/19 06:00
MHDA- 2013/10/23 06:00
PMCR- 2013/02/17
CRDT- 2013/02/19 06:00
PHST- 2012/12/04 00:00 [received]
PHST- 2013/01/30 00:00 [accepted]
PHST- 2013/02/19 06:00 [entrez]
PHST- 2013/02/19 06:00 [pubmed]
PHST- 2013/10/23 06:00 [medline]
PHST- 2013/02/17 00:00 [pmc-release]
AID - 1742-2094-10-28 [pii]
AID - 10.1186/1742-2094-10-28 [doi]
PST - epublish
SO  - J Neuroinflammation. 2013 Feb 17;10:28. doi: 10.1186/1742-2094-10-28.