Thymosin beta 4 prevents systemic lipopolysaccharide-induced plaque load in middle-age APP/PS1 mice

Othman, Othman; Marshall, Hayley J.; Masterson, Mitchell; Winlow, Poppy; Gibson, Graham M.; Ding, Yuchun; Pardon, Marie‐Christine

doi:10.1016/j.intimp.2023.109951

Cited by 1 publication

(1 citation statement)

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“…Tβ 4 has also demonstrated neuroprotective and neurorestorative potential within various neurological injury models [20]. In particular, the neuroprotective effects of Tβ4 have been observed in a mouse model of neuroinflammatory BBB dysfunction induced by systemic infection with LPS [21,22]. However, since Tβ 4 cannot directly pass through the BBB [20], it is believed that these effects are mediated outside of the central nervous system, affecting the body as a whole.…”

Section: Introductionmentioning

confidence: 99%

Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106–126) via Neurotrophic Factor Signaling

2023

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Prion protein peptide (PrP) has demonstrated neurotoxicity in brain cells, resulting in the progression of prion diseases with spongiform degenerative, amyloidogenic, and aggregative properties. Thymosin beta 4 (Tβ4) plays a role in the nervous system and may be related to motility, axonal enlargement, differentiation, neurite outgrowth, and proliferation. However, no studies about the effects of Tβ4 on prion disease have been performed yet. In the present study, we investigated the protective effect of Tβ4 against synthetic PrP (106–126) and considered possible mechanisms. Hippocampal neuronal HT22 cells were treated with Tβ4 and PrP (106–126) for 24 h. Tβ4 significantly reversed cell viability and reactive oxidative species (ROS) affected by PrP (106–126). Apoptotic proteins induced by PrP (106–126) were reduced by Tβ4. Interestingly, a balance of neurotrophic factors (nerve growth factor and brain-derived neurotrophic factor) and receptors (nerve growth factor receptor p75, tropomyosin related kinase A and B) were competitively maintained by Tβ4 through receptors reacting to PrP (106–126). Our results demonstrate that Tβ4 protects neuronal cells against PrP (106–126) neurotoxicity via the interaction of neurotrophic factors/receptors.

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