Neuroprotective effect and underlying mechanism of sodium danshensu [3-(3,4-dihydroxyphenyl) lactic acid from Radix and Rhizoma Salviae miltiorrhizae = Danshen] against cerebral ischemia and reperfusion injury in rats |
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| Institution: | 1. Department of Obstetrics and Gynecology, Nagoya University, School of Medicine, Nagoya, Japan;2. Department of Fetal and Maternal Medicine, Nagara Medical Center, Gifu City, Japan;3. Biostatics Laboratory, Nagoya University, School of Medicine, Nagoya, Japan;1. College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, China;2. Department of PET/CT Center, The First Affiliated Hospital, School of Medicine, Zhejiang University Zhejiang 310003, China;3. Department of Pharmacy, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, China;4. Department of Neurology, Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, Zhejiang 310009, China;1. Institute of Materia Medica, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China;2. Department of Surgery, University of Toronto, Toronto, ON, Canada |
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| Abstract: | Sodium danshensu (SDSS), the sodium salt of danshensu (DSS), has the same pharmacological effects as DSS. In the present study, we aimed to investigate the neuroprotective effect and possible mechanism of SDSS against cerebral ischemic/reperfusion injury. Sprague-Dawley rats were randomly divided into four groups: sham, control, 30 mg/kg and 60 mg/kg SDSS. Cerebral ischemia was induced by 2 h of middle cerebral artery occlusion (MCAO). Neurological functional deficits were evaluated according to the modified neurological severity score (mNSS); cerebral infarct volume and histological damage were measured by TTC or H–E staining. In addition, the number of apoptotic cells and caspase 3/7 activity were assessed by TUNEL or Caspase-Glo assay. And the expression of apoptosis-regulatory proteins and the PI3K/Akt pathway were investigated by western blotting. Our results showed that treatment with SDSS for 5 days after MCAO remarkably improved neurologic deficits and survival rate, reduced infarct volume and the number of dead neurons. SDSS also decreased the number of apoptotic cells, regulated the expression of Bcl-2 and Bax, and increased the ratio of Bcl-2/Bax. Further study revealed that treatment with SDSS also increased the level of p-Akt and p-GSK-3β. Taken together, our results suggest that SDSS has the neuroprotective effect against cerebral I/R injury, and the potential mechanism might to inhibition of apoptosis through activating the PI3K/Akt signal pathway. |
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