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Rosmarinic acid protects against experimental diabetes with cerebral ischemia: relation to inflammation response.
J Neuroinflammation. 2013 Feb 17; 10:28.JN

Abstract

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-α (TNF-α) 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-α-induced nuclear transcription factor κB (NF-κB) 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-κB 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-κB signaling pathway.

Authors+Show Affiliations

School of Pharmaceutical Sciences and Institute of Material Medica, Binzhou Medical University, Yantai 264003, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23414442

Citation

Luan, Haiyun, et al. "Rosmarinic Acid Protects Against Experimental Diabetes With Cerebral Ischemia: Relation to Inflammation Response." Journal of Neuroinflammation, vol. 10, 2013, p. 28.
Luan H, Kan Z, Xu Y, et al. Rosmarinic acid protects against experimental diabetes with cerebral ischemia: relation to inflammation response. J Neuroinflammation. 2013;10:28.
Luan, H., Kan, Z., Xu, Y., Lv, C., & Jiang, W. (2013). Rosmarinic acid protects against experimental diabetes with cerebral ischemia: relation to inflammation response. Journal of Neuroinflammation, 10, 28. https://doi.org/10.1186/1742-2094-10-28
Luan H, et al. Rosmarinic Acid Protects Against Experimental Diabetes With Cerebral Ischemia: Relation to Inflammation Response. J Neuroinflammation. 2013 Feb 17;10:28. PubMed PMID: 23414442.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosmarinic acid protects against experimental diabetes with cerebral ischemia: relation to inflammation response. AU - Luan,Haiyun, AU - Kan,Zechun, AU - Xu,Yong, AU - Lv,Changjun, AU - Jiang,Wanglin, Y1 - 2013/02/17/ PY - 2012/12/04/received PY - 2013/01/30/accepted PY - 2013/2/19/entrez PY - 2013/2/19/pubmed PY - 2013/10/23/medline SP - 28 EP - 28 JF - Journal of neuroinflammation JO - J Neuroinflammation VL - 10 N2 - 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-α (TNF-α) 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-α-induced nuclear transcription factor κB (NF-κB) 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-κB 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-κB signaling pathway. SN - 1742-2094 UR - https://www.unboundmedicine.com/medline/citation/23414442/Rosmarinic_acid_protects_against_experimental_diabetes_with_cerebral_ischemia:_relation_to_inflammation_response_ L2 - https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-10-28 DB - PRIME DP - Unbound Medicine ER -