Baicalin Induces Differential Expression of Cytochrome <i>C</i> Oxidase in Human Lung H441 Cell

Cheng, Kur‐Ta; Hou, Wen Chi; Huang, Yu‐Chen; Wang, Leng-Fang

doi:10.1021/jf0301549

Cited by 12 publications

(10 citation statements)

References 18 publications

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“…Primer-BLAST was used to design primers that detect the exogenous and endogenous TSPO mRNA (Table S2). The primers for COX IV subunit 2 PCR were used according to a previous publication 68 (Table S2). Diluted cDNA (1 µl) was added to 4 µl of reaction mixture containing 2.5 µl of SsoFast supermix (BioRad) and forward and reverse primers at a final concentration of 0.5 µM each.…”

Section: Methodsmentioning

confidence: 99%

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Functional gains in energy and cell metabolism after TSPO gene insertion

et al. 2017

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Recent loss-of-function studies in tissue-specific as well as global Tspo (Translocator Protein 18 kDa) knockout mice have not confirmed its long assumed indispensability for the translocation of cholesterol across the mitochondrial inter-membrane space, a rate-limiting step in steroid biosynthesis. Instead, recent studies in global Tspo knockout mice indicate that TSPO may play a more fundamental role in cellular bioenergetics, which may include the indirect down-stream regulation of transport or metabolic functions. To examine whether overexpression of the TSPO protein alters the cellular bioenergetic profile, Jurkat cells with low to absent endogenous expression were transfected with a TSPO construct to create a stable cell line with de novo expression of exogenous TSPO protein. Expression of TSPO was confirmed by RT-qPCR, radioligand binding with [3H]PK11195 and immunocytochemistry with a TSPO antibody. We demonstrate that TSPO gene insertion causes increased transcription of genes involved in the mitochondrial electron transport chain. Furthermore, TSPO insertion increased mitochondrial ATP production as well as cell excitability, reflected in a decrease in patch clamp recorded rectified K channel currents. These functional changes were accompanied by an increase in cell proliferation and motility, which were inhibited by PK11195, a selective ligand for TSPO. We suggest that TSPO may serve a range of functions that can be viewed as downstream regulatory effects of its primary, evolutionary conserved role in cell metabolism and energy production.

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Section: Methodsmentioning

confidence: 99%

“…β-actin ( ACTB ) 68 as well as glyceraldehyde 3-phosphate dehydrogenase ( GAPDH ) 69 were used as internal standards (i.e. housekeeping genes (Table S2)).…”

Section: Methodsmentioning

confidence: 99%

Functional gains in energy and cell metabolism after TSPO gene insertion

et al. 2017

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“…1. Baicalin has recently been reported to exhibit antioxidant activity by inhibiting lipid peroxidation (Ng et al, 2000;Gao et al, 2003;Chan et al, 2000;Cheng et al, 2003). In addition, its anti-hyperglycemic effects in streptozotocin-induced diabetic Wistar rats have also been recently reported (Li et al, 2010;Waisundara et al, 2009aWaisundara et al, , 2009b.…”

Section: Introductionmentioning

confidence: 98%

Baicalin upregulates the genetic expression of antioxidant enzymes in Type-2 diabetic Goto-Kakizaki rats

et al. 2011

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“…In human lung H441 cell, baicalin induced differential expression of cytocheome c oxidase, and elevated cAMP consequently (Cheng et al 2003). cAMP is a key second messenger in amiloride-sensitive ENaC-mediated sodium reabsorption.…”

Section: Discussionmentioning

confidence: 96%

Effects of baicalin on alveolar fluid clearance and α-ENaC expression in rats with LPS-induced acute lung injury

Deng

Wang

Liang

et al. 2017

Can. J. Physiol. Pharmacol.

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Baicalin has been reported to attenuate lung edema in the process of lung injury. However, the effect of baicalin on alveolar fluid clearance (AFC) and epithelial sodium channel (ENaC) expression has not been tested. Sprague-Dawley rats were anesthetized and intratracheally injected with either 1 mg/kg lipopolysaccharide (LPS) or saline vehicle. Baicalin with various concentrations (10, 50, and 100 mg/kg) was injected intraperitoneally 30 min before administration of LPS. Then lungs were isolated for measurement of AFC, cyclic adenosine monophosphate (cAMP) level, and cellular localization of α-ENaC. Moreover, mouse alveolar type II (ATII) epithelial cell line was incubated with baicalin (30 μmol/L), adenylate cyclase inhibitor SQ22536 (10 μmol/L), or cAMP-dependent protein kinase inhibitor (PKA) KT5720 (0.3 μmol/L) 15 min before LPS (1 μg/mL) incubation. Protein expression of α-ENaC was detected by Western blot. Baicalin increased cAMP concentration and AFC in a dose-dependent manner in rats with LPS-induced acute lung injury. The increase of AFC induced by baicalin was associated with an increase in the abundance of α-ENaC protein. SQ22536 and KT5720 prevented the increase of α-ENaC expression caused by baicalin in vitro. These findings suggest that baicalin prevents LPS-induced reduction of AFC by upregulating α-ENaC protein expression, which is activated by stimulating cAMP/PKA signaling pathway.

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Baicalin Induces Differential Expression of Cytochrome C Oxidase in Human Lung H441 Cell

Cited by 12 publications

References 18 publications

Functional gains in energy and cell metabolism after TSPO gene insertion

Functional gains in energy and cell metabolism after TSPO gene insertion

Baicalin upregulates the genetic expression of antioxidant enzymes in Type-2 diabetic Goto-Kakizaki rats

Effects of baicalin on alveolar fluid clearance and α-ENaC expression in rats with LPS-induced acute lung injury

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