The Possible Inhibition Effect of Lycium barbarum Polysaccharides on Rat Intracerebral Hemorrhage Secondary Neuronal Apoptosis through Intervening Endogenous/Exogenous Pathways of Apoptosis

Autor: Yourui Zou, ShengYu Sun, Usama Ilyas Sharif, Abdul Wasie, Hui Ma
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Indian Journal of Neurosurgery, Vol 9, Iss 02, Pp 106-114 (2020)
Druh dokumentu: article
ISSN: 2277-954X
2277-9167
DOI: 10.1055/s-0040-1713059
Popis: Objective The aim of this study was to explore the inhibition effect and possible mechanism of Lycium barbarum polysaccharides (LBP) on rat intracerebral hemorrhage (ICH) secondary neuronal apoptosis. Materials and Methods High-, medium-, and low-dose LBP (50, 100, and 200 mg•kg) and nimodipine (10 mg•kg) groups were given once daily by 15-day gavage before operation, while the sham operation and ICH groups were given the equal volume of saline. An ICH model was established by autologous blood injection and the neurological function in each group was scored at 4, 8, 12, 24, and 48 hours after modeling. Furthermore, terminal deoxynucleotidyl transferase dUTP nick end labeling analysis was performed to detect neuronal apoptosis, while western blot, immunohistochemistry, and real-time-polymerase chain reaction were used to study the influence of LBP on ICH secondary neuronal apoptosis. Results The neurological function score was significantly decreased after ICH, and the intervention effect of a single drug was not evident. The apoptotic nerve cells increased significantly in the ICH group but decreased considerably in the LBP groups. Furthermore, tumor necrosis factor alpha (TNF-α) expression decreased significantly, while B-cell lymphoma 2 expression increased substantially in the high- and medium-dose LBP groups compared with ICH group, suggesting that LBP could reduce the effect of ICH. However, the impact of LBP did not correlate positively with the dose. Conclusion The application of LBP may not significantly improve neurological function after ICH, but it can inhibit rat ICH secondary neuronal apoptosis.
Databáze: Directory of Open Access Journals
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