Treatment with MQA, a Derivative of Caffeoylquinic Acid, Provides Neuroprotective Effects against Cerebral Ischemia Through Suppression of the p38 Pathway and Oxidative Stress in Rats

• Published in: Journal of molecular neuroscience Vol. 67; no. 4; pp. 604 - 612
• Main Authors: Chen, Long, Liu, Dan-ni, Wang, Yu, Liu, Xue-ying, Han, Shuai, Zhang, Ke, Li, Guo-yu, Tian, Xing, Wang, Hang-yu, Wang, Jin-hui
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.04.2019; Springer Nature B.V
• Subjects: AKT protein; Apoptosis; BAX protein; Bcl-2 protein; Biomedical and Life Sciences; Biomedicine; Brain injury; Caffeoylquinic acid; Caspase; Caspase-3; Cell Biology; Cerebral blood flow; Cortex; DNA nucleotidylexotransferase; Glutathione; Glutathione peroxidase; Immunohistochemistry; In vivo methods and tests; Injuries; Ischemia; Malic acid; Malondialdehyde; Neurochemistry; Neurology; Neuroprotection; Neurosciences; Nitric oxide; Nitric-oxide synthase; Occlusion; Oxidative stress; Peroxidase; Proteins; Proteomics; Quinic acid; Rodents; Western blotting; Neuroprotection; Cerebral ischemia; Caffeoylquinic acid; Apoptosis
• ISSN: 0895-8696; 1559-1166
• DOI: 10.1007/s12031-019-01268-1

1,5- O -dicaffeoyl-3- O -(4-malic acid methylester)–quinic acid (MQA), extracted from Arctium lappa L ., has been observed to exert neuroprotective effects in vitro. The aim of this study was to investigate whether MQA is an effective therapeutic method for cerebral ischemic injury in vivo. In this study, adult male rats were randomly divided into four groups: a normal group, a model group subjected to middle cerebral artery occlusion (MCAO) for 24 h, a model + MQA group (which received intragastric MQA for the 7 days prior to MCAO), and a model + positive drug group. MQA appeared to induce effects in cerebral ischemic injury in rats, by downregulating malondialdehyde, glutathione peroxidase, and nitric oxide synthase levels. Treatment with MQA significantly reduced infarcted sections. In addition, caspase-3 and Iba1 protein expression were evaluated with immunohistochemistry, and cortical cell apoptosis was assessed with terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays. Expression of AKT and Bax, ERK1/2, P38 and Bcl-2, NFkB 1 , PARP, and caspase-3 was assessed with Western blotting. We found Bcl-2 and NFkB 1 (p 50 ) expressions were upregulated, whereas the expression of PARP, caspase-3, NFkB 1 (p 105 ), ERK1/2, P38, AKT, and Bax was downregulated. In conclusion, we observed MQA was an effective treatment for cerebral ischemic injury in rats.