ABSTRACT
BACKGROUND: Cerebral apoplexy patients are prone to cognitive impairment, and it is very important to choose appropriate treatment methods to improve their cognitive impairment after stroke. AIM: To evaluate the effects of enhanced external counterpulsation (EECP) in conjunction with atorvastatin on cognitive function, neurotransmitter levels, and the repair of brain tissue damage in patients with cognitive impairment due to stroke. METHODS: In this retrospective study, data from 60 patients with poststroke cognitive impairment due to stroke who were treated in our hospital from February 2021 to July 2022 were analyzed and divided into a treatment group (n = 30) and a control group (n = 30) according to the different nursing methods applied. Patients in the treatment group received EECP in addition to atorvastatin, while those in the control group received atorvastatin alone. Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and activities of daily living (ADL) scale scores were compared between the two groups. Additionally, the two groups were compared in terms of serum acetylcholine (ACh), acetylcholinesterase (AChE), nitric oxide (NO), endothelin-1 (ET-1), ß2-microglobulin (ß2-MG), glial fibrillary acidic protein (GFAP), and visinin-like protein 1 (VILIP-1) in the serum. Blood flow measurements from the anterior cerebral artery (ACA), middle cerebral artery (MCA) and posterior cerebral artery (PCA) were compared between the two groups before and after treatment, and the pulsatility index (PI) and resistance index (RI) of each artery were determined. RESULTS: MMSE, MoCA, and ADL scores all improved in both groups following treatment, with the study group showing more improvement than the control group (P < 0.05). After treatment, there were statistically significant increases in both ACh and NO levels, whereas decreases occurred in AChE, ET-1, ß2-MG, VILIP-1, and GFAP, levels and the PI and RI of the left-ACA, right-ACA, left-MCA, right-MCA, left-PCA, and right-PCA. The study group showed greater gains in all metrics than the control group (P < 0.05). CONCLUSION: EECP combined with atorvastatin is effective in the treatment of cognitive impairment after stroke and can effectively improve the cognitive function, neurotransmitter levels, and brain tissue damage status of patients.
ABSTRACT
Human Nestin (hNestin) has been found to express in melanoma, and its expression is positively correlated with the advanced stage of melanoma. However, the precise role of hNestin in the development of melanoma has not been fully understood. The present study aimed to explore the role of hNestin in the proliferation and invasion of melanoma cells. The lentivirus vector carrying a short hairpin RNAs (shRNAs) targeting hNestin (hNestin-shRNA-LV) was stably infected into human melanoma cells UACC903, which expressed high levels of hNestin. The effects of hNestin knockdown on the proliferation, apoptosis, migration of melanoma cells and the related signaling pathways were investigated by immunofluorence, Western blotting and reverse transcription polymerase chain reaction (RT-PCR), respectively. The results showed that hNestin was expressed in most melanoma specimens and the melanoma cells studied. Knockdown of hNestin expression significantly inhibited the proliferation of melanoma cells, blocked the formation of cell colony, arrested cell cycle at G1/S stage and suppressed the activation of Akt and GSK3ß. hNestin-silent cells also showed a sheet-like appearance with tight cell-cell adhesion, decreased membrane expression of N-cadherin and ß-catenin, and attenuated migration. Furthermore, hNestin silence resulted in the inhibition of tumor growth in vivo. Our study indicates that hNestin knockdown suppresses the proliferation of melanoma cells, which might be through affecting Akt-GSK3ß-Rb pathway-mediated G1/S arrest, and hNestin silence inhibits the migration by selectively modulating the expression of cell adhesion molecules in the process of epithelial-mesenchymal transition.
Subject(s)
Gene Expression Regulation, Neoplastic , Glycogen Synthase Kinase 3 beta/genetics , Melanoma/genetics , Nestin/genetics , Proto-Oncogene Proteins c-akt/genetics , Retinoblastoma Protein/genetics , Skin Neoplasms/genetics , Antigens, CD/genetics , Antigens, CD/metabolism , Apoptosis , Cadherins/genetics , Cadherins/metabolism , Cell Line, Tumor , Cell Movement , Cell Proliferation , Epithelial-Mesenchymal Transition , G1 Phase Cell Cycle Checkpoints , Genetic Vectors/chemistry , Genetic Vectors/metabolism , Glycogen Synthase Kinase 3 beta/metabolism , Humans , Lentivirus/genetics , Lentivirus/metabolism , Melanoma/metabolism , Melanoma/pathology , Melanoma/therapy , Nestin/antagonists & inhibitors , Nestin/metabolism , Proto-Oncogene Proteins c-akt/metabolism , RNA, Small Interfering/genetics , RNA, Small Interfering/metabolism , Retinoblastoma Protein/metabolism , Signal Transduction , Skin Neoplasms/metabolism , Skin Neoplasms/pathology , Skin Neoplasms/therapy , Tumor Burden , Xenograft Model Antitumor Assays , beta Catenin/genetics , beta Catenin/metabolismABSTRACT
Human Nestin (hNestin) has been found to express in melanoma,and its expression is positively correlated with the advanced stage of melanoma.However,the precise role of hNestin in the development of melanoma has not been fully understood.The present study aimed to explore the role of hNestin in the proliferation and invasion of melanoma cells.The lentivirus vector carrying a short hairpin RNAs (shRNAs) targeting hNestin (hNestin-shRNA-LV) was stably infected into human melanoma cells UACC903,which expressed high levels of hNestin.The effects of hNestin knockdown on the proliferation,apoptosis,migration of melanoma cells and the related signaling pathways were investigated by immunofluorence,Western blotting and reverse transcription polymerase chain reaction (RT-PCR),respectively.The results showed that hNestin was expressed in most melanoma specimens and the melanoma cells studied.Knockdown of hNestin expression significantly inhibited the proliferation of melanoma cells,blocked the formation of cell colony,arrested cell cycle at G1/S stage and suppressed the activation of Akt and GSK3β.hNestin-silent cells also showed a sheet-like appearance with tight cell-cell adhesion,decreased membrane expression of N-cadherin and β-catenin,and attenuated migration.Furthermore,hNestin silence resulted in the inhibition of tumor growth in vivo.Our study indicates that hNestin knockdown suppresses the proliferation of melanoma cells,which might be through affecting Akt-GSK3β-Rb pathway-mediated G1/S arrest,and hNestin silence inhibits the migration by selectively modulating the expression of cell adhesion molecules in the process of epithelial-mesenchymal transition.
