Universität zu Köln

Li, Li, Tan, Hong-Ping, Liu, Cheng-Yong, Yu, Lin-Tao, Wei, Da-Nian, Zhang, Zi-Chen, Lu, Kui, Zhao, Ke-Sen, Maegele, Marc, Cai, Dao-Zhang and Gu, Zheng-Tao (2019). Polydatin prevents the induction of secondary brain injury after traumatic brain injury by protecting neuronal mitochondria. Neural Regen. Res., 14 (9). S. 1573 - 1583. MUMBAI: WOLTERS KLUWER MEDKNOW PUBLICATIONS. ISSN 1876-7958

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Abstract

Polydatin is thought to protect mitochondria in different cell types in various diseases. Mitochondrial dysfunction is a major contributing factor in secondary brain injury resulting from traumatic brain injury. To investigate the protective effect of polydatin after traumatic brain injury, a rat brain injury model of lateral fluid percussion was established to mimic traumatic brain injury insults. Rat models were intra-peritoneally injected with polydatin (30 mg/kg) or the SIRT1 activator SRT1720 (20 mg/kg, as a positive control to polydatin). At 6 hours post-traumatic brain injury insults, western blot assay was used to detect the expression of SIRT1, endoplasmic reticulum stress related proteins and p38 phosphorylation in cerebral cortex on the injured side. Flow cytometry was used to analyze neuronal mitochondrial superoxide, mitochondrial membrane potential and mitochondrial permeability transition pore opened. Ultrastructural damage in neuronal mitochondria was measured by transmission electron microscopy. Our results showed that after treatment with polydatin, release of reactive oxygen species in neuronal mitochondria was markedly reduced; swelling of mitochondria was alleviated; mitochondrial membrane potential was maintained; mitochondrial permeability transition pore opened. Also endoplasmic reticulum stress related proteins were inhibited, including the activation of p-PERK, spliced XBP-1 and cleaved ATF6. SIRT1 expression and activity were increased; p38 phosphorylation and cleaved caspase-9/3 activation were inhibited. Neurological scores of treated rats were increased and the mortality was reduced compared with the rats only subjected to traumatic brain injury. These results indicated that polydatin protectrd rats from the consequences of traumatic brain injury and exerted a protective effect on neuronal mitochondria. The mechanisms may be linked to increased SIRT1 expression and activity, which inhibits the p38 phosphorylation-mediated mitochondrial apoptotic pathway.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Li, Li UNSPECIFIED UNSPECIFIED UNSPECIFIED Tan, Hong-Ping UNSPECIFIED UNSPECIFIED UNSPECIFIED Liu, Cheng-Yong UNSPECIFIED UNSPECIFIED UNSPECIFIED Yu, Lin-Tao UNSPECIFIED UNSPECIFIED UNSPECIFIED Wei, Da-Nian UNSPECIFIED UNSPECIFIED UNSPECIFIED Zhang, Zi-Chen UNSPECIFIED UNSPECIFIED UNSPECIFIED Lu, Kui UNSPECIFIED UNSPECIFIED UNSPECIFIED Zhao, Ke-Sen UNSPECIFIED UNSPECIFIED UNSPECIFIED Maegele, Marc UNSPECIFIED UNSPECIFIED UNSPECIFIED Cai, Dao-Zhang UNSPECIFIED UNSPECIFIED UNSPECIFIED Gu, Zheng-Tao UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-143736
DOI:	10.4103/1673-5374.255972
Journal or Publication Title:	Neural Regen. Res.
Volume:	14
Number:	9
Page Range:	S. 1573 - 1583
Date:	2019
Publisher:	WOLTERS KLUWER MEDKNOW PUBLICATIONS
Place of Publication:	MUMBAI
ISSN:	1876-7958
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language ENDOPLASMIC-RETICULUM STRESS; SEVERE HEMORRHAGIC-SHOCK; ARTERIAL SMOOTH-MUSCLE; APOPTOSIS; ISCHEMIA; SIRT1; NEUROPROTECTION; HYPOTHERMIA; INHIBITION; DAMAGE Multiple languages Cell Biology; Neurosciences Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/14373