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Olive leaf extract inhibits lead poisoning-induced brain injury

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Neural Regeneration Research 2013年第22期8卷 2021-2029页

作者： Yu Wang Shengqing Wang Wenhui Cui Jiujun He Zhenfu Wang Xiaolu Yang Department of Biology and Chemistry Longnan Teachers College

Olive leaves have an antioxidant capacity, and olive leaf extract can protect the blood, spleen and hippocampus in lead-poisoned mice. However, little is known about the effects of olive leaf extract on lead-induced brain injury. This study was designed to determine whether olive leaf extract can inhibit lead-induced brain injury, and whether this effect is associated with antioxidant capacity. First, we established a mouse model of lead poisoning by continuous intragastric administration of lead acetate for 30 days. Two hours after successful model establishment, lead-poisoned mice were given olive leaf extract at doses of 250, 500 or 1 000 mg/kg daily by intragastric administration for 50 days. Under the transmission electron microscope, olive leaf extract attenuated neuronal and capillary injury and reduced damage to organelles and the matrix around the capillaries in the frontal lobe of the cerebral cortex in the lead-poisoned mice. Olive leaf extract at a dose of 1 000 mg/kg had the greatest protective effect. Spectrophotometry showed that olive leaf extract significantly in- creased the activities of superoxide dismutase, catalase, alkaline phosphatase and acid phes- phatase, while it reduced malondialdehyde content, in a dose-dependent manner. Furthermore, immunohistochemical staining revealed that olive leaf extract dose-dependently decreased Bax protein expression in the cerebral cortex of lead-poisoned mice. Our findings indicate that olive leaf extract can inhibit lead-induced brain injury by increasing antioxidant capacity and reducing apop- tosis.

关键词： neural regeneration traditional Chinese medicine olive leaf extract lead brain injury superoxidedismutase catalase alkaline phosphatase acid phosphatase malondialdehyde apoptosis neu-ropathology grants-supported paper neuroregeneration

Hydrogen-rich saline injection into the subarachnoid cavity within 2 weeks promotes recovery after acute spinal cord injury

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Neural Regeneration Research 2015年第6期10卷 958-964页

作者： Jian-long Wang Qing-shan Zhang Kai-di Zhu Jian-feng Sun Ze-peng Zhang Jian-wen Sun Ke-xiang Zhang Department of Orthopedics the Third Xiangya Hospital of Central South University

Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich saline would promote the repair of spinal cord injury induced by Allen＇s method in rats. At 0.5, 1, 2, 4, 8, 12 and 24 hours after injury, then once daily for 2 weeks, 0.25 mL/kg hydrogen-rich saline was infused into the subarachnoid space through a catheter. Results at 24 hours, 48 hours, 1 week and 2 weeks after injury showed that hydrogen-rich saline markedly reduced cell death, inflammatory cell infiltration, serum malondialdehyde content, and caspa se-3 immunoreactivity, elevated serum superoxide dismutase activity and calcitonin gene-related peptide immunoreactivity, and improved motor function in the hindlimb. The present study confirms that hydrogen-rich saline injected within 2 weeks of injury effectively contributes to the repair of spinal cord injury in the acute stage.

关键词： nerve regeneration spinal cord injury hydrogen-rich saline reactive oxygen species physiological saline oxidative stress Basso, Beattie and Bresnahan score malondialdehyde superoxidedismutase calcitonin gene-related peptide caspase-3 neural regeneration

Neuroprotective effects of daidzein on focal cerebral ischemia injury in rats

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Neural Regeneration Research 2015年第1期10卷 146-152页

作者： Adem Bozkurt Aras Mustafa Guven Tar?k Akman Adile Ozkan Halil Murat Sen Ugur Duz Y?ld?ray Kalkan Coskun Silan Murat Cosar Department of Neurosurgery Canakkale Onsekiz Mart University Department of Neurology Canakkale Onsekiz Mart University Department of Medical Biochemistry Ministry of HealthAdministration of Public Health Deparment of Histology and Embryology Recep Tayyip Erdo?an UniversityFaculty of Medicine Department of Pharmacology Canakkale Onsekiz Mart University

Daidzein, a plant extract, has antioxidant activity. It is hypothesized, in this study, that daidzein exhibits neuroprotective effects on cerebral ischemia. Rat models of middle cerebral artery oc- clusion were intraperitoneally administered daidzein. Biochemical and immunohistochemical tests showed that superoxide dismutase and nuclear respiratory factor 1 expression levels in the brain tissue decreased after ischemia and they increased obviously after daidzein administra- tion; malondialdehyde level and apoptosis-related cysteine peptidase caspase-3 and caspase-9 immunoreactivity in the brain tissue increased after ischemia and they decreased obviously after daidzein administration. Hematoxylin-eosin staining and luxol fast blue staining results showed that intraperitoneal administration of daidzein markedly alleviated neuronal damage in the ischemic brain tissue. These findings suggest that daidzein exhibits neuroprotective effects on ischemic brain tissue by decreasing oxygen free radical production, which validates the afore- mentioned hypothesis.

关键词： nerve regeneration brain ischemia stroke daidzein oxidative stress apoptosis superoxidedismutase malondialdehyde nuclear respiratory factor 1 neural regeneration

Givinostat inhibition of hepatic stellate cell proliferation and protein acetylation

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World Journal of Gastroenterology 2015年第27期21卷 8326-8339页

作者： Yu-Gang Wang Ling Xu Ting Wang Jue Wei Wen-Ying Meng Na Wang Min Shi Department of Gastroenterology Shanghai Tongren Hospital Affiliated to Shanghai Jiao Tong University School of Medicine

AIM: To explore the effect of the histone deacetylase inhibitor givinostat on proteins related to regulation of hepatic stellate cell ***: The cell counting kit-8 assay and flow cytometry were used to observe changes in proliferation, apoptosis, and cell cycle in hepatic stellate cells treated with givinostat. Western blot was used to observe expression changes in p21, p57, CDK4, CDK6, cyclin D1, caspase-3, and caspase-9 in hepatic stellate cells exposed to givinostat. The scratch assay was used to analyze the effect of givinostat on cell migration. Effects of givinostat on the reactive oxygen species profile, mitochondrial membrane potential, and mitochondrial permeability transition pore opening in JS-1 cells were observed by laser confocal ***: Givinostat significantly inhibited JS-1 cell proliferation and promoted cell apoptosis, leading to cell cycle arrest in G0/G1 phases. Treatment with givinostat downregulated protein expression of CDK4, CDK6, and cyclin D1, whereas expression of p21 and p57 was significantly increased. The givinostat-induced apoptosis of hepatic stellate cells was mainly mediatedthrough p38 and extracellular signal-regulated kinase 1/2. Givinostat treatment increased intracellular reactive oxygen species production, decreased mitochondrial membrane potential, and promoted mitochondrial permeability transition pore opening. Acetylation of superoxide dismutase(acetyl K68) and nuclear factor-κB p65(acetyl K310) was upregulated, while there was no change in protein expression. Moreover, the notable beneficial effect of givinostat on liver fibrosis was also confirmed in the mouse ***: Givinostat has antifibrotic activities via regulating the acetylation of nuclear factor-κB and superoxide dismutase 2, thus inhibiting hepatic stellate cell proliferation and inducing apoptosis.

关键词： Givinostat Hepatic stellate cells Histonedeacetylase inhibitor Nuclear factor-κB superoxidedismutase