The neuroprotective effects of Lutongkeli in traumatic brain injury rats by anti-apoptosis mechanism.

Purpose: To explore the neuroprotective effects of Lutongkeli (LTKL) in traumatic brain injury (TBI) and detect the related mechanism.

Methods: TBI model was established with LTKL administration (2 and 4 g/kg/d, p.o.

Protein phosphorylation: A potential target in glioma development.

Glioma is one of the most common primary brain tumors, and mortality due to this disease is second only to cardiovascular and cerebrovascular diseases. In traditional surgery, it is difficult to eradicate glioma; often recurrence increases its malignant degree, leading to a large number of patients killed by this disease. It is one of the most important subjects to study its pathogenesis and explore effective treatment methods.

BDNF promotes neuronal survival after neonatal hypoxic-ischemic encephalopathy by up-regulating Stx1b and suppressing VDAC1.

Neonatal hypoxic-ischemic encephalopathy (HIE), is a major cause of neurologic disorders in terms of neonates, with the unclear underlying mechanisms. In the study, triphenyl tetrazolium chloride (TTC) staining and Zea-longa score were performed to examine the neurologic damage in hypoxia and ischemia (HI) rats. The results showed that HI induced obviously infarct and serious neurologic impairment in neonatal rats.

Vof-16 knockout improves the recovery from hypoxic-ischemic brain damage of neonatal rats.

Hypoxic-ischemic encephalopathy (HIE) results in high neonatal mortality and severe neurological impairments, and its underlying molecular mechanism underwent extensive investigations. Long non-coding RNA (lncRNA) is considered to be an important regulator on brain development and many neurological diseases. Currently, little is known about the role of Vof-16 (lncRNA) in HIE.

bFGF promotes neurological recovery from neonatal hypoxic-ischemic encephalopathy by IL-1β signaling pathway-mediated axon regeneration.

Introduction: Neonatal hypoxia-ischemic brain damage (HIBD) can lead to serious neuron damage and dysfunction, causing a significant worldwide health problem. bFGF as a protective reagent promotes neuron repair under hypoxia/ischemia (HI). However, how bFGF and downstream molecules were regulated in HI remains elusive.