Li-Dan-He-Ji Improves Infantile Cholestasis Hepatopathy Through Inhibiting Calcium-Sensing Receptor-Mediated Hepatocyte Apoptosis

Qin, Huan; Zhang, Lingling; Xiong, Xiaoli; Jiang, Zhixia; Xiao, Chen; Zhang, Linli; Wang, Yuji; Wu, Yuntao; Qiu, Yanyan; Zhou, Ling; Yan, Su-Qi

doi:10.3389/fphar.2020.00156

Cited by 9 publications

(2 citation statements)

References 45 publications

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“…Furthermore, LINC00152-silencing significantly increased the protein expression levels of Bax and caspase-3 and downregulated those of Bcl-2. Bax, caspase-3 and Bcl-2 are considered to be key mediators of cell apoptosis in several diseases (2,29,30). Emerging evidence has supported that Bax and caspase-3 are proapoptotic proteins (31), while Bcl-2 upregulation inhibits cell apoptosis (32).…”

Section: Discussionmentioning

confidence: 99%

LINC00152 knockdown suppresses tumorigenesis in non-small cell lung cancer via sponging miR-16-5p

Hu¹,

Chen²,

Chen³

et al. 2022

J Thorac Dis

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Background: Non-small cell lung cancer (NSCLC) is one of the most aggressive types of cancer worldwide. It has been reported that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of NSCLC. In addition, LINC00152 is known to be upregulated in NSCLC. However, the mechanism underlying the effect of LINC00152 on NSCLC tumorigenesis remains to be elucidated. Methods:In the present study, cell viability, apoptosis and invasion were investigated by CCK-8, flow cytometry and Transwell assays, respectively. Reverse transcription-quantitative polymerase chain reaction and Western blotting were performed to determine the mRNA and protein expression levels. In addition, the association between LINC00152, microRNA (miR)-16-5p and BCL2-like 2 (BCL2L2) was evaluated using a dual-luciferase assay. Results:The results demonstrated that LINC00152-knockdown significantly attenuated the viability of NSCLC cells via promoting cell apoptosis. In addition, the migration and invasion ability of NSCLC cells was also decreased following transfection of cells with LINC00152 siRNA. Furthermore, miR-16-5p inhibitor or BCLCL2-overexpression reversed LINC00152 siRNA-induced NSCLC cell growth inhibition. Conclusions:The findings of the present study demonstrated that LINC00152-silencing suppressed NSCLC tumorigenesis via regulating the miR-16-5p/BCL2L2 axis. Therefore, linc00152 has the potential as a molecular marker and may be a potential target for the treatment of non-small cell lung cancer.

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Section: Discussionmentioning

confidence: 99%

LINC00152 knockdown suppresses tumorigenesis in non-small cell lung cancer via sponging miR-16-5p

Hu¹,

Chen²,

Chen³

et al. 2022

J Thorac Dis

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“…Furthermore, while infantile cholestasis caused by toxic bile acids results in liver damage and mortality, the role of calcium signaling in this pathophysiology is still unknown. Specifically, calcium-sensing receptors are elevated during infantile cholestasis, and their elevation enhances the activation of p-extracellular signal-regulated kinase (p-ERK) which in turn lessens the expression of apoptotic markers, lowers intracellular calcium, and also inhibits the development of oxidative stress ( Qin et al, 2020 ). As summarized in Figure 2 , cyclosporine can induce cell injury by mediating ROS generation due to interorganelle communication.…”

Section: Introductionmentioning

confidence: 99%

Involvement of oxidative species in cyclosporine-mediated cholestasis

et al. 2022

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Cyclosporine is an established medication for the prevention of transplant rejection. However, adverse consequences such as nephrotoxicity, hepatotoxicity, and cholestasis have been associated with prolonged usage. In cyclosporine-induced obstructive and chronic cholestasis, for example, the overproduction of oxidative stress is significantly increased. Additionally, cyclosporine exerts adverse effects on liver function and redox balance responses in treated rats, as evidenced by its increasing levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin while also decreasing the levels of glutathione and NADPH. Cyclosporine binds to cyclophilin to produce its therapeutic effects, and the resulting complex inhibits calcineurin, causing calcium to accumulate in the mitochondria. Accumulating calcium with concomitant mitochondrial abnormalities induces oxidative stress, perturbation in ATP balance, and failure of calcium pumps. Also, cyclosporine-induced phagocyte oxidative stress generation via the interaction of phagocytes with Toll-like receptor-4 has been studied. The adverse effect of cyclosporine may be amplified by the release of mitochondrial DNA, mediated by oxidative stress-induced mitochondrial damage. Given the uncertainty surrounding the mechanism of cyclosporine-induced oxidative stress in cholestasis, we aim to illuminate the involvement of oxidative stress in cyclosporine-mediated cholestasis and also explore possible strategic interventions that may be applied in the future.

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Hepatoprotective effect of forsythiaside a against acetaminophen-induced liver injury in zebrafish: Coupling network pharmacology with biochemical pharmacology

Gong

Zhou

Wang

et al. 2021

Journal of Ethnopharmacology

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Li-Dan-He-Ji Improves Infantile Cholestasis Hepatopathy Through Inhibiting Calcium-Sensing Receptor-Mediated Hepatocyte Apoptosis

Cited by 9 publications

References 45 publications

LINC00152 knockdown suppresses tumorigenesis in non-small cell lung cancer via sponging miR-16-5p

LINC00152 knockdown suppresses tumorigenesis in non-small cell lung cancer via sponging miR-16-5p

Involvement of oxidative species in cyclosporine-mediated cholestasis

Hepatoprotective effect of forsythiaside a against acetaminophen-induced liver injury in zebrafish: Coupling network pharmacology with biochemical pharmacology

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