Protective effects and mechanism of TPX2 on neurocyte apoptosis of rats in Alzheimer's disease model

Abstract

We investigated the protective effects and mechanism of TPX2 on apoptosis of rat neurocytes. A total of 90 SD rats were randomly divided into the drug group, the control group and the blank group, with 30 rats in each group. The rats in the drug group and in the blank group were anesthetized with 10% chloral hydrate (at the dose of 0.5 ml/100 g) and Aβ1–42, with the concentration of 5 µl (1 µg/µl), was injected in the exact position of bilateral hippocampal areas of rats to establish the model. The configured TPX2 inhibitors and edible benne oil were mixed and made into a suspension. After model establishment, the rats were given different treatment methods; the rats in the drug group were given gavage administration in the proportion of 75 mg/kg once a day. The rats in the control group were given intragastric administration with the same proportion of physiological saline once a day. The blank group was the normal healthy group and the rats in this group did not undergo any surgery or drug treatment. Brain tissue in rats were divided into two parts, one part was fixed, dehydrated, paraffin-embedded and made into slices of approximately 5 µm. TUNEL staining was used to examine the apoptosis of brain tissue, H&E staining was used to observe the brain tissue cells of each group, and western blotting for detecting the MAPK, Erk and expression levels of p38 and RT-polymerase chain reaction method was employed to examine mRNA expression levels of MAPK, Erk and p21. After one week, TUNEL staining showed that apoptosis of brain tissue in the drug group was significantly greater than those of the control and blank groups. The protein expression levels of MAPK, Erk and p38 were significantly higher than those of the control group and the normal healthy group; the differences were statistically significant (P<0.05). Western blotting showed that the protein expression levels of MAPK, Erk and p38 of the drug group were significantly lower than those of the control group but higher than those of the normal healthy group; the differences were statistically significant (P<0.05). TPX2 has a protective effect on the apoptosis of brain tissue processed by Aβ1–42, which plays its role through the inhibition of the protein expression levels of MAPK, Erk and p38.

((E)-N-(4-(((2-Amino-5-phenylpyridin-3-yl)imino)methyl)pyridin-2-yl)cyclopropanecarboxamide) Ameliorated Aβ1–42-Induced Alzheimer’s Disease in SD Rats by Inhibiting Oxidative Stress and Apoptosis

“…Numerous studies have shown that neuronal apoptosis is a key factor leading to neuron loss and progressive AD development. − Apoptotic DNA fragments can be seen in the brain tissue of AD patients, and a significant increase in TUNEL-positive cells was observed in the brain tissue upon autopsy of AD patients . In this study, serious neuronal apoptosis was found in the hippocampus of the SD rat brain after microinjection of Aβ 1–42 , which indicated the existence of neuronal apoptosis during AD.…”

Single cell molecular alterations reveal target cells and pathways of concussive brain injury

“…9f ) and T4 reversed the TBI-induced changes of 93 genes (Fig. 9g ), including Ttr , Wdr72 (implicated in cognitive processing speed 53 ), and Tpx2 (protective of neurocyte apoptosis in an AD model 54 ) (Fig. 9h ).…”

Matrine prevents the early development of hepatocellular carcinoma like lesions in rat liver

“…Each group of rats were sacrificed in 3 batches at 2, 4 and 7 weeks after hepatectomy. At the end of the administration period, animals ate and drank freely for 4 h. The rats were anesthetized by intraperitoneal injection of 10% chloral hydrate (300 mg/kg), then they were killed by extirpation of eyeballs and exsanguination (26–28). They were confirmed dead by observation of respiratory and cardiac arrest and the absence of any pain response to needle puncture of the extremities.…”