Grape Seed Proanthocyanidin Extract Down-Regulates Autophagic Proteins (LC3II and Beclin-1) in a Mouse Model of Neonatal Hypoxic-Ischemic Brain Injury
Clinical Medicine Research
Volume 8, Issue 1, January 2019, Pages: 16-20
Received: Jan. 31, 2019;
Accepted: Mar. 11, 2019;
Published: Mar. 25, 2019
Views 178 Downloads 29
Li Luo, School of Biosciences & Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Xing Tu, School of Biosciences & Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Wei Liu, School of Clinical Medicine, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Xuexia Zhang, Department of Anesthesiology, the Fifth Affiliated Hospital, Sun Yat-Sen University, Zhuhai, People's Republic of China
Yilin Liu, School of Clinical Medicine, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Wenyan Zhao, School of Clinical Medicine, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Junhua Yang, School of Biosciences & Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Mengxia Wang, Intensive Care Unit, Guangdong No. 2 Provincial People's Hospital, Guangzhou, People's Republic of China
Jing Liu, School of Biosciences & Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, People's Republic of China
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe brain disease that often leads to death or irreversible sequelae. The aim of this study was to determine the effect of a naturally active drug (grape seed proanthocyanidin extract [GSPE]) on the expression of autophagic proteins in a mouse model of neonatal hypoxic-ischemic brain injury. In this study immunofluorescence staining and Western blotting were used to detect the expression of autophagy markers (LC3II and beclin1) in the brains of neonatal mice with hypoxic-ischemic brain injuries after GSPE administration. Our study showed that GSPE pre-treatment down-regulates LC3II and beclin-1 expression, thus GSPE may be a potential drug for the treatment of HIE.
Grape Seed Proanthocyanidin Extract Down-Regulates Autophagic Proteins (LC3II and Beclin-1) in a Mouse Model of Neonatal Hypoxic-Ischemic Brain Injury, Clinical Medicine Research.
Vol. 8, No. 1,
2019, pp. 16-20.
Liu X M, Feng Y and Li A M (2014). Nerve protective effect of Baicalin on newborn HIBD rats. Asian Pac J Trop Med 7: 806-810.
Dai Y, Li W, Zhong M, Chen J, Cheng Q., Liu Y, and Li T (2017). The paracrine effect of cobalt chloride on BMSCs during cognitive function rescue in the HIBD rat. Behav Brain Res 332: 99-109.
Xu B, Xiao A, Chen W, Turlova E, Liu R, Barszczyk A, Sun C, Liu L, Tymianski M, Feng Z and Sun H (2016). Neuroprotective effects of a PSD-95 inhibitor in neonatal hypoxic-ischemic brain injury. Mol Neurobi, 53: 5962-5970.
Liu G, Li Z G and Gao J S (2017). Hypothermia in neonatal hypoxic-ischemic encephalopathy (HIE). Eur Rev Med Pharmacol Sci 21: 50-53.
Rao R, Trivedi S, Distler A, Liao S, Vesoulis Z, Smyser C, and Mathur A M (2019). Neurodevelopmental Outcomes in Neonates with Mild Hypoxic Ischemic Encephalopathy Treated with Therapeutic Hypothermia. American journal of perinatology. doi: 10.1055/s-0038-1676973.
Liu B, Zhang H, Tan X, Yang D, Lv Z, Jiang H, Lu J, Baiyun R and Zhang Z (2017). GSPE reduces lead-induced oxidative stress by activating the Nrf2 pathway and suppressing miR153 and GSK-3β in rat kidney. Oncotarget 8: 42226-42237.
Niu L, Shao M, Liu Y, Hu J, Li R, Xie H, Zhou L, Shi L, Zhang R and Niu Y (2017). Reduction of oxidative damages induced by titanium dioxide nanoparticles correlates with induction of the Nrf2 pathway by GSPE supplementation in mice. Chem Biol Interact 275: 133-144.
Wei M, Guo F, Rui D, Wang H, Feng G, Li S, and Song G (2018). Alleviation of Arsenic-Induced Pulmonary Oxidative Damage by GSPE as Shown during In vivo and In vitro Experiments. Biol Trace Elem Res 183: 80-91.
Muzzi M, Buonvicino D, Urru M, Tofani L and Chiarugi A (2018). Repurposing of dexpramipexole to treatment of neonatal hypoxic/ischemic encephalopathy. Neurosci lett 687: 234-240.
Santa-Maria I, Diaz-Ruiz C, Ksiezak-Reding H, Chen A, Ho L, Wang J and Pasinetti G M (2012). GSPE interferes with tau aggregation in vivo: implication for treating tauopathy. Neurobiol Aging 33: 2072-2081.
Taniguchi H and Andreasson K (2008). The hypoxic ischemic encephalopathy model of perinatal ischemia. JoVE 21: e955-e955.
Liu X M, Feng Y and Li A M (2015). Effect of G–CSF and TPO on HIBD in neonatal rats. Asian Pac J Trop Med 8: 132-136.
Fang M, Jiang H, Ye L, Cai C, Hu Y, Pan S, Li P, Xiao J and Lin Z (2017). Metformin treatment after the hypoxia-ischemia attenuates brain injury in newborn rats. Oncotarget 8: 75308-75325.
Bano S, Chaudhary V, and Garga U C (2017). Neonatal hypoxic-ischemic encephalopathy: A radiological review. J Pediatr Neurosci 12: 1-6.
Lee B S, Jung E, Lee Y, and Chung S H (2017). Hypothermia decreased the expression of heat shock proteins in neonatal rat model of hypoxic ischemic encephalopathy. Cell Stress and Chaperones 22: 409-415.
Nair J and Kumar, V (2018). Current and Emerging Therapies in the Management of Hypoxic Ischemic Encephalopathy in Neonates. Children 5: 99.
Zheng Z, Zhang L, Qu Y, Xiao G, Li S, Bao S, Lu R and Mu D (2018). Mesenchymal stem cells protect against hypoxia‐ischemia brain damage by enhancing autophagy through BDNF/mTOR signaling pathway. STEM CELLS 36: 1109-1121.
Hara T, Nakamura K, Matsui M, Yamamoto A, Nakahara Y and Suzuki-Migishima R (2006). Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice. Nature 441: 885-889.
Ye L, Feng Z, Doycheva D, Malaguit J, Dixon B, Xu N, Zhang J and Tang J (2018). Cpg-odn exerts a neuroprotective effect via the tlr9/pampk signaling pathway by activation of autophagy in a neonatal hie rat model. Experimental Neurology 301: 70-80.
Li P, Hao L, Guo YY, Yang G L, Mei H, Li X H and Zhai Q (2018). Chloroquine inhibits autophagy and deteriorates the mitochondrial dysfunction and apoptosis in hypoxic rat neurons. Life Sciences 202: 70-77.