PMID- 23344852 OWN - NLM STAT- MEDLINE DCOM- 20130912 LR - 20211021 IS - 1573-6903 (Electronic) IS - 0364-3190 (Linking) VI - 38 IP - 4 DP - 2013 Apr TI - Intrathecal epigallocatechin gallate treatment improves functional recovery after spinal cord injury by upregulating the expression of BDNF and GDNF. PG - 772-9 LID - 10.1007/s11064-013-0976-5 [doi] AB - This study aimed to investigate the therapeutic effects of epigallocatechin-3-gallate (EGCG) administered by subarachnoid injection following spinal cord injury (SCI) in rats and to explore the underlying mechanism. Sprague-Dawley rats were randomly divided into four groups of 12 as follows: a sham group (laminectomy only); a control group; a 10 mg/kg EGCG-treated group; and a 20 mg/kg EGCG-treated group. SCI was induced in the rats using the modified weight-drop method (10 g x 4 cm) at the T10 (10th thoracic vertebral) level. EGCG (10 or 20 mg/kg) or vehicle as control was administered by subarachnoid injection at lumbar level 4 immediately after SCI. Locomotor functional recovery was assessed during the four weeks post-operation using open-field locomotor tests and inclined-plane tests. At the end of the study, the segments of spinal cord encompassing the injury site were removed for histopathological analysis. Immunohistochemical and Western blot analyses were performed to observe the expression of: the B cell CLL/lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). The results showed that the EGCG-treated animals had significantly better recovery of locomotor function, less myelin loss, greater Bcl-2 expression and attenuated Bax expression. In addition, the EGCG treatment significantly increased the expression of BDNF and GDNF after SCI. These findings suggest that EGCG treatment can significantly improve locomotor recovery, and this neuroprotective effect may be related to the up-regulation of BDNF and GDNF, and the inhibition of apoptosis-related proteins. Therefore, EGCG may be a promising therapeutic agent for SCI. FAU - Tian, Wei AU - Tian W AD - Department of Spine Surgery, Beijing Jishuitan Hospital, No 31, Xinjiekou East Street, Xicheng District, Beijing, People's Republic of China. jstspine@126.com FAU - Han, Xiao-Guang AU - Han XG FAU - Liu, Ya-Jun AU - Liu YJ FAU - Tang, Guo-Qing AU - Tang GQ FAU - Liu, Bo AU - Liu B FAU - Wang, Yong-Qing AU - Wang YQ FAU - Xiao, Bin AU - Xiao B FAU - Xu, Yun-Feng AU - Xu YF LA - eng PT - Journal Article DEP - 20130124 PL - United States TA - Neurochem Res JT - Neurochemical research JID - 7613461 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Glial Cell Line-Derived Neurotrophic Factor) RN - 0 (Neuroprotective Agents) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (bcl-2-Associated X Protein) RN - 8R1V1STN48 (Catechin) RN - BQM438CTEL (epigallocatechin gallate) SB - IM EIN - Neurochem Res. 2020 Jul;45(7):1729-1730. PMID: 32323106 MH - Animals MH - Apoptosis/drug effects MH - Brain-Derived Neurotrophic Factor/*biosynthesis MH - Catechin/*analogs & derivatives/pharmacology/therapeutic use MH - Female MH - Glial Cell Line-Derived Neurotrophic Factor/*biosynthesis MH - Motor Activity/drug effects MH - Neuroprotective Agents/*pharmacology MH - Proto-Oncogene Proteins c-bcl-2/biosynthesis MH - Rats MH - Rats, Sprague-Dawley MH - Recovery of Function/drug effects MH - Spinal Cord/drug effects MH - Spinal Cord Injuries/*drug therapy/*physiopathology MH - bcl-2-Associated X Protein/biosynthesis EDAT- 2013/01/25 06:00 MHDA- 2013/09/13 06:00 CRDT- 2013/01/25 06:00 PHST- 2012/09/26 00:00 [received] PHST- 2013/01/17 00:00 [accepted] PHST- 2013/01/14 00:00 [revised] PHST- 2013/01/25 06:00 [entrez] PHST- 2013/01/25 06:00 [pubmed] PHST- 2013/09/13 06:00 [medline] AID - 10.1007/s11064-013-0976-5 [doi] PST - ppublish SO - Neurochem Res. 2013 Apr;38(4):772-9. doi: 10.1007/s11064-013-0976-5. Epub 2013 Jan 24.