Thymosin-β4 Attenuates Ethanol-induced Neurotoxicity in Cultured Cerebral Cortical Astrocytes by Inhibiting Apoptosis

Yang, Hao; Cui, Guang-Bin; Jiao, Xi-Ying; Wang, Jian; Ju, Gong; You, Song

doi:10.1007/s10571-009-9439-6

Cited by 13 publications

(10 citation statements)

References 62 publications

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“…77 Although we did not investigate apoptosis in the present study, Tβ4 provides the neuroprotection likely through its anti-apoptotic effect. Tβ4 reduces apoptosis in many cells including human corneal epithelial cells 24 and gingival fibroblasts, 54 rat cortical astrocytes 81 and neurons. 11 Intracerebroventricular administration of Tβ4 significantly reduces hippocampal neuronal loss induced by kainic acid.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats

Xiong¹,

Zhang²,

Mahmood³

et al. 2012

JNS

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Object Thymosin beta 4 (Tβ4) is a regenerative multifunctional peptide. This study will test the hypothesis that Tβ4 treatment initiated 6 hours post-injury reduces brain damage and improves functional recovery in rats after traumatic brain injury (TBI). Methods TBI was induced by controlled cortical impact over the left parietal cortex. Young adult male Wistar rats with TBI were randomly divided into the following groups: 1) Saline group (n=7); 2) Tβ4-6 mg/kg group (n=8), and 3) Tβ4-30 mg/kg group (n=8). Tβ4 or saline was administered intraperitoneally starting at 6 hours post-injury and then repeated daily at 24 and 48 hours. An additional group of sham animals underwent surgery without injury (n=6). Sensorimotor function and spatial learning were assessed using a modified neurological severity score and Morris water maze tests, respectively. Animals were sacrificed 35 days after injury and brain sections processed to assess lesion volume, hippocampal cell loss, cell proliferation and neurogenesis after Tβ4 treatment. Results Compared to saline, Tβ4 treatment initiated 6 hours post-injury significantly improved sensorimotor functional recovery and spatial learning, reduced cortical lesion volume and hippocampal cell loss, and enhanced cell proliferation and neurogenesis in the injured hippocampus. The high dose of Tβ4 showed better beneficial effects compared to the low-dose treatment. Conclusions Tβ4 treatment initiated 6 hours post-injury provides both neuroprotection and neurorestoration after TBI, indicating that Tβ4 has promising therapeutic potential in TBI patients. These data warrant further investigation of the optimal dose and therapeutic window of Tβ4 treatment for TBI and the associated underlying mechanisms.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats

Xiong¹,

Zhang²,

Mahmood³

et al. 2012

JNS

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show abstract

“…Thymosin beta‐4 has also been shown to offset ethanol‐induced neurotoxicity in cultured cortical astrocytes through inhibition of apoptosis signaling (Yang et al . ). One of the mechanisms underlying the capacity of thymosin beta‐4 to suppress apoptosis may in part be because of its anti‐peroxidation effect.…”

Section: Discussionmentioning

confidence: 97%

“…; Yang et al . , ; Philp and Kleinman ) and is considered a candidate neurorestorative agent (Morris et al . ).…”

Section: Discussionmentioning

confidence: 99%

Comparative peptidomics analysis of neural adaptations in rats repeatedly exposed to amphetamine

Romanova

Lee

Kelleher

et al. 2012

Journal of Neurochemistry

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Repeated exposure to amphetamine (AMPH) induces long-lasting behavioral changes, referred to as sensitization, that are accompanied by various neuroadaptations in the brain. To investigate the chemical changes that occur during behavioral sensitization, we applied a comparative proteomics approach to screen for neuropeptide changes in a rodent model of AMPH-induced sensitization. By measuring peptide profiles with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and comparing signal intensities using principal component analysis and variance statistics, subsets of peptides are found with significant differences in the dorsal striatum, nucleus accumbens and medial prefrontal cortex of AMPH-sensitized male Sprague-Dawley rats. These biomarker peptides, identified in follow-up analyses using liquid chromatography and tandem mass spectrometry, suggest that behavioral sensitization to AMPH is associated with complex chemical adaptations that regulate energy/metabolism, neurotransmission, apoptosis, neuroprotection, and neuritogenesis, as well as cytoskeleton integrity and neuronal morphology. Our data contribute to a growing number of reports showing that in addition to the mesolimbic dopamine system, which is the best known signaling pathway involved with reinforcing the effect of psychostimulants, concomitant chemical changes in other pathways and in neuronal organization may play a part in the overall effect of chronic AMPH exposure on behavior.

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“…Tβ4 could inhibit cell apoptosis by regulating the expression of Bcl-2 and Caspase-3. Many studies have proven the efficacy of Tβ4 to inhibit cell apoptosis on various tissue and cells [ 19 , 20 ]. There are also many studies verifying that Tβ4 have significant anti-apoptosis effect on corneal tissue [ 21 , 22 ].…”

Section: Discussionmentioning

confidence: 99%

Protection effect of thymosin β4 on ethanol injury in corneal stromal keratocyte

Liu

Guo²,

Peng³

et al. 2022

BMC Ophthalmol

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Purpose To investigate the protective effects of thymosin β4 (Tβ4) on ethanol injured human corneal keratocytes (HCKs). Methods HCKs and BALB/c mice were chosen as the study subject. Ethanol was used to treat the cells and corneal stroma of mice to build the ethanol injured model in vitro and vivo respectively. CCK-8 was used to evaluate the cell metabolic activity. DCFH-DA was used to detect the intracellular reactive oxygen species level. TUNEL was chose to detect the cell apoptosis rate. The cell proliferation and migration were investigated by using wound healing insert. Wound healing of corneal surface and stroma was observed by using fluorescein sodium eyedrop and HE stain. RT-qPCR, ELISA, and immunostaining were performed to detect gene and protein expression in keratocytes or corneal stroma tissue of mice. Results Ethanol induced oxidative stress injury and cell apoptosis on HCKs, and Tβ4 can alleviate it by up-regulating the expression of Bcl-2, catalase, and CuZnSOD, and inhibiting the expression of Caspase-3. Tβ4 promotes the proliferation of HCKs and the process of corneal wound healing. It may relevant to the up-regulated expression of Ki67. Conclusions Our study established an ethanol-injured corneal stroma model in both vitro and vivo. The present study confirmed that Tβ4 play a protective effect on the reconstruction process of ethanol-injured corneal stroma.

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Thymosin-β4 Attenuates Ethanol-induced Neurotoxicity in Cultured Cerebral Cortical Astrocytes by Inhibiting Apoptosis

Cited by 13 publications

References 62 publications

Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats

Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats

Comparative peptidomics analysis of neural adaptations in rats repeatedly exposed to amphetamine

Protection effect of thymosin β4 on ethanol injury in corneal stromal keratocyte

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