RESUMO
PURPOSE: Cuproptosis-related long non-coding RNA (lncRNA) diseases are associated with the occurrence and development of tumors. This study aimed to investigate whether cuproptosis-related lncRNA can predict the prognosis of patients with lung adenocarcinoma (LUAD). METHODS: Cuproptosis-related lncRNA prognosis (CLPS) model was successfully constructed through cox regression and lasso regression analyses. Then, the prognostic value of CLPS model was tested through the survival analysis, the ROC curve and the nomogram. Finally, the correlation of CLPS model with tumor immunity and tumor mutation burden was analyzed, and the potential susceptibility of drugs for LUAD were predicted. RESULTS: CLPS model for LUAD (AC090948.1, CRIM1-DT, AC026356.2, AC004832.5, AL161431.1) was successfully constructed, which has an independent prognostic value. Furthermore, the risk score of CLPS model was correlated with tumor immune characteristics and immune escape, which can predict the sensitivity of drugs including Cisplatin, Etoposide, Gemcitabine, and Erlotinib. CONCLUSIONS: In conclusion, it was found that CLPS model was associated with tumor immunity and tumor mutation load, which also predicted four potentially sensitive drugs for LUAD patients at different risks.
Assuntos
Adenocarcinoma , Apoptose , RNA Longo não Codificante , Humanos , Adenocarcinoma/genética , Pulmão , Nomogramas , Prognóstico , RNA Longo não Codificante/genética , CobreRESUMO
Abstract Introduction: The objective of this study is to investigate the protective effect of kaempferol against ischemia/reperfusion (IR) injury and the underlying molecular mechanisms. Methods: H9C2 cells were pretreated with kaempferol for 24 hours and further insulted with IR injury. Cell vitality, reactive oxygen species (ROS) level, glutathione (GSH) level, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and sirtuin-3 (SIRT3), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) expressions were evaluated. Moreover, short interfering ribonucleic acid targeting SIRT3 was used to investigate the role of SIRT3 against IR mediated by kaempferol in vitro. IR mice models were also established to confirm the protective effects of kaempferol on IR in vivo. Results: After IR injury, H9C2 cells vitality was reduced, ROS levels, NADPH oxidase activity, and Bax expressions were increased, and GSH levels and Bcl2 expressions were decreased. After kaempferol pretreatment, the vitality of H9C2 cells was increased. The levels of ROS, NADPH oxidase activity, and Bax expression were decreased. In addition, levels of GSH and Bcl2 expression were enhanced. Furthermore, silencing SIRT3 attenuated the protective effect mediated by kaempferol, with increased ROS levels, NADPH oxidase activity, and Bax expression, along with reduced GSH level and Bcl2 expression. In vivo IR model showed that kaempferol could preserve IR-damaged cardiac function. Conclusion: Kaempferol has the capability of attenuating H9C2 cells IR injury through activating SIRT3 to inhibit oxidative stress.
RESUMO
INTRODUCTION: The objective of this study is to investigate the protective effect of kaempferol against ischemia/reperfusion (IR) injury and the underlying molecular mechanisms. METHODS: H9C2 cells were pretreated with kaempferol for 24 hours and further insulted with IR injury. Cell vitality, reactive oxygen species (ROS) level, glutathione (GSH) level, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and sirtuin-3 (SIRT3), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) expressions were evaluated. Moreover, short interfering ribonucleic acid targeting SIRT3 was used to investigate the role of SIRT3 against IR mediated by kaempferol in vitro. IR mice models were also established to confirm the protective effects of kaempferol on IR in vivo. RESULTS: After IR injury, H9C2 cells vitality was reduced, ROS levels, NADPH oxidase activity, and Bax expressions were increased, and GSH levels and Bcl2 expressions were decreased. After kaempferol pretreatment, the vitality of H9C2 cells was increased. The levels of ROS, NADPH oxidase activity, and Bax expression were decreased. In addition, levels of GSH and Bcl2 expression were enhanced. Furthermore, silencing SIRT3 attenuated the protective effect mediated by kaempferol, with increased ROS levels, NADPH oxidase activity, and Bax expression, along with reduced GSH level and Bcl2 expression. In vivo IR model showed that kaempferol could preserve IR-damaged cardiac function. CONCLUSION: Kaempferol has the capability of attenuating H9C2 cells IR injury through activating SIRT3 to inhibit oxidative stress.