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The Protective Effect and Mechanism of Baicalin on Postoperative Cognitive Function and Nerves in Aged Rats

Author(s): Liangyu Cai, Hongmei Zhou, R. H. Li, C. H. Jiang, M. Y. Xu and J. N. Zhang*
Department of Anesthesiology, 1Department of Pain, Traditional Chinese Medicine Hospital of Wuxi, Wuxi, Jiangsu 214071, P. R. China

Correspondence Address:
J. N. Zhang, Department of Anesthesiology, Traditional Chinese Medicine Hospital of Wuxi, Wuxi, Jiangsu 214071, P. R. China, E-mail:

To explore the effect of baicalin on cognitive function and nerves after splenectomy in aged rats is the main objective of the study. Aged rats were randomly divided into a sham operation group, a model group (to construct a splenectomy surgical model) and a baicalin treatment group (baicalin was given after the model was constructed). The pathological conditions like interleukin-6, tumor necrosis factor alpha, interleukin-1 beta content; brain detection by terminal deoxynucleotidyl transferase dUTP nick end labeling method apoptosis of tissue cell; western blot method was used to detect the expression of related proteins and real-time fluorescence quantitative polymerase chain reaction method was used to detect the messenger ribonucleic acid levels of related genes. Compared with the control group, the brain tissue cell apoptosis increased and the expression of inflammatory factors increased in the model group; compared with the model group, the brain tissue apoptosis of the baicalin treatment group decreased, the expression of Ki67 positive cells increased and the inflammation-related factor interleukin-6, tumor necrosis factor alpha, interleukin-1 beta levels were significantly decreased, N-methyl D-aspartate receptor subtype 2B, phosphorylated-extracellular signal-regulated kinase, phosphorylated-cAMP response element-binding protein expressions were significantly increased. Baicalin can improve postoperative cognitive dysfunction and nerve injury in aged rats after splenectomy by improving the pathological state of brain tissue, attenuating the inflammatory response and promoting apoptosis of brain tissue.

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Citations : 66710

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