Gonadal steroids block the calpain-1-dependent intrinsic pathway of apoptosis in an experimental rat stroke model

Vahidinia, Zeinab; Atlasi, Mohammad Ali; Naderian, Homayoun; Beyer, Cordian; Tameh, Abolfazl Azami

doi:10.1080/01616412.2016.1250459

Cited by 27 publications

(10 citation statements)

References 58 publications

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Section: Resultsmentioning

confidence: 99%

“…As far as is known, apoptosis plays a decisive role in mediating cell death through two major signaling pathways: the intrinsic pathway mediated by Cyto C release from mitochondria to stimulate caspase-9, and the extrinsic apoptotic pathway originating from the activation of cell surface death receptor (DR) and stimulating caspase-8. 21 Therefore, the activities of Caspase-3, -8, and -9 in the cells was determined in this study. The results showed that the activities of Caspase-3 (7.04 ± 0.61), Caspase-8 (10.92 ± 1.31), and Caspase-9 (8.87 ± 0.73) in Ad-PLCγ2 shRNA transfected group were lower than that those the blank control and Ad-dull groups, with significant difference (P < 0.05).…”

Section: Plcγ2 Silncing Inhibits Cell Apoptosis Through Extrinsic and Intrinsic Pathwaysmentioning

confidence: 99%

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Silencing of phospholipase C gamma 2 promotes proliferation of rat hepatocytes in vitro

Chen

Zhu

Liu

et al. 2018

J of Cellular Biochemistry

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The management of hepatic failure is undoubtedly difficult, and poor results have led to the search for novel therapeutic approaches. Nowadays, anti-apoptotic gene therapy is considered as an ideal approach. It has been proved that phospholipase Cγ2 (PLCγ2) is involved in the apoptosis of immune cells and tumor cells; however, whether this gene is related to hepatocyte death is still unclear. This study examined the role of PLCγ2 by inhibiting its expression in rat hepatocytes with siRNA. We also further analyzed the cellular mechanism by which the expression inhibition of PLCγ2 induces cell death. Silencing PLCγ2 gene by adenovirus vector expressing PLCγ2-targeted siRNA caused the great decline in the number of G1- and G2/M phase cells, the significant increase in the number of S phase cells, and the obvious reduction in apoptosis index. In addition, silencing PLCγ2 gene relieved the rat hepatocyte damage, such as the cell shrinkage and chromatin condensation, nuclear fragmentation. Further analysis of Ad-PLCγ2 siRNA-transfected hepatocytes demonstrated that suppression of PLCγ2 gene expression could cause the caspase dependent cell death by inhibiting the signal pathway MEKK1/MKK4/JNK1/2/c-Jun. In conclusion, these findings suggest that interference with PLCγ2 expression could relieve the inhibitory effect of PLCγ2 on hepaocyte apoptosis, thus, promote proliferation through inactivating PKCδ-mediated JNK1/2 signaling pathway.

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Section: Resultsmentioning

confidence: 99%

Section: Plcγ2 Silncing Inhibits Cell Apoptosis Through Extrinsic and Intrinsic Pathwaysmentioning

confidence: 99%

Silencing of phospholipase C gamma 2 promotes proliferation of rat hepatocytes in vitro

Chen

Zhu

Liu

et al. 2018

J of Cellular Biochemistry

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“…Infarct size. as described in previous studies (22,23), after reperfusion for 48 h, the animals were anesthetized by intraperitoneal injection of 10% chloral hydrate (400 mg/kg) and then decapitated. The brain was rapidly removed, and the coronal section of brain was sliced in a special groove (thickness: 2 mm) after cooling in ice-cold saline for 10 min.…”

Section: Methodsmentioning

confidence: 99%

Intracarotid cold saline infusion contributes to neuroprotection in MCAO‑induced ischemic stroke in rats via serum and glucocorticoid‑regulated kinase 1

Wang

Huang

et al. 2019

Mol Med Report

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intracarotid cold saline infusion (icSi) brings about neuroprotective effects in ischemic stroke. However, the involvement of serum and glucocorticoid-regulated kinase 1 (SGK1) in the underlying mechanism of icSi is not fully understood; therefore, we used the rat middle cerebral artery occlusion (Mcao) model to investigate the neuroprotective effects of icSi on ischemic stroke in rats, as well as the involvement of SGK1 in these effects. icSi decreased infarct size and brain swelling, as determined by 2,3,5-triphenyltetrazolium chloride staining and the dry-wet weight method, respectively. The results of terminal deoxynucleotidyl transferase mediated nick end labeling (Tunel) and nissl staining showed that icSi also suppressed apoptosis and increased the relative integral optical density (iod) values of nissl bodies in the rat Mcao model. regarding the mechanism, the results of immunohistochemistry and western blotting revealed that icSi upregulated SGK1 expression and downregulated beclin-1 and lc-3 expression in the rat Mcao model. in addition, SGK1 knockdown increased icSi-mediated infarct size and brain swelling, promoted apoptosis, and reduced the iod values of nissl bodies in the rat Mcao model. in addition, we found that SGK1 knockdown upregulated beclin-1 and lc-3 expression mediated by icSi. overall, icSi had a neuroprotective effect on ischemic stroke after reperfusion by upregulating SGK1 and inhibiting autophagy.

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“…Although used extensively in stroke research, there is limited knowledge of how TTC-treated rat brain sections are altered and if they can be used for quantitative immunohistochemical detection after staining with TTC. Regardless, several studies have used TTC stained brain sections for immunohistochemical studies [7, 8] and quantification of proteins using fluorescence intensity [4, 9–12] without considering the potential effects of TTC on the immunohistochemical composite staining, including autofluorescence, nonspecific secondary antibody fluorescence, and primary antibody detection. Thus, we investigated whether TTC-treated rat brain sections were altered and if they could be used for quantitative immunohistochemical detection.…”

Section: Introductionmentioning

confidence: 99%

Effect of TTC Treatment on Immunohistochemical Quantification of Collagen IV in Rat Brains after Stroke

Bishop

Chan

et al. 2018

Transl. Stroke Res.

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Although used extensively in stroke research, there is limited knowledge of how 2, 3, 5-triphenyltetrazolium chloride (TTC)-treated rat brain sections are altered and if they can be used for immunohistochemical quantification after staining with TTC. In the present study, we hypothesized that TTC treatment (TTC+) would not interfere with collagen IV immunohistochemical staining compared with non-TTC-treated (TTC-) brain slices. We further hypothesized that there would be no difference in autofluorescence or nonspecific secondary antibody fluorescence between TTC+ and TTC- brain slices. Coronal brain sections of male Wistar rats (n = 5/group) were either treated with TTC or not after middle cerebral artery occlusion or sham surgery, and processed for immunohistochemical staining with mouse anti-collagen IV as the primary antibody, and goat anti-IgM as the secondary antibody. Four images were taken in the cerebral cortex of the contralateral side of infarction in each brain slice using an Olympus BX50 fluorescence microscope, and average intensity of the entire image was quantified using the Metamorph software. Compared with TTC- brain slices, TTC+ brain slices showed a significantly lower autofluorescence (P < 0.05), but was unchanged for nonspecific secondary antibody fluorescence. In addition, TTC+ brain slices had similar collagen IV staining intensity compared with TTC- brain slices. These results demonstrate that TTC+ brain slices are usable for immunohistochemical quantification.

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Gonadal steroids block the calpain-1-dependent intrinsic pathway of apoptosis in an experimental rat stroke model

Abstract: We conclude that a combined steroid treatment inhibits ischemia-induced neuronal apoptosis through the regulation of intrinsic pathways.

Cited by 27 publications

References 58 publications

Silencing of phospholipase C gamma 2 promotes proliferation of rat hepatocytes in vitro

Silencing of phospholipase C gamma 2 promotes proliferation of rat hepatocytes in vitro

Intracarotid cold saline infusion contributes to neuroprotection in MCAO‑induced ischemic stroke in rats via serum and glucocorticoid‑regulated kinase 1

Effect of TTC Treatment on Immunohistochemical Quantification of Collagen IV in Rat Brains after Stroke

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