Attenuation of cytotoxicity induced by tBHP in H9C2 cells by Bacopa monniera and Bacoside A

T, Mohan Manu; Anand, T.; Khanum, Farhath

doi:10.1016/j.pathophys.2018.03.002

Cited by 13 publications

(2 citation statements)

References 32 publications

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“…To further investigate the relationship between ROS, autophagy flux, and ER-stress induced apoptosis in neuronal cells, we examined whether ROS accumulation induces lysosomal dysfunction and subsequent autophagy flux blockade and ER stress-induced apoptosis in neural cells in vitro . ROS was generated by TBHP treatment to causes oxidative damage via oxidation of membrane lipids and release of lipid peroxidation product MDA 34 . Then, we used the fluorescent probe DCFH-DA, a ROS indicator, to detect the intracellular ROS levels in PC12 cells.…”

Section: Resultsmentioning

confidence: 99%

TFE3, a potential therapeutic target for Spinal Cord Injury via augmenting autophagy flux and alleviating ER stress

Zhou

Zheng

et al. 2020

Theranostics

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Background and Aim: Increasing evidence suggests that spinal cord injury (SCI)-induced defects in autophagic flux may contribute to an impaired ability for neurological repair following injury. Transcription factor E3 (TFE3) plays a crucial role in oxidative metabolism, lysosomal homeostasis, and autophagy induction. Here, we investigated the role of TFE3 in modulating autophagy following SCI and explored its impact on neurological recovery. Methods: Histological analysis via HE, Nissl and Mason staining, survival rate analysis, and behavioral testing via BMS and footprint analysis were used to determine functional recovery after SCI. Quantitative real-time polymerase chain reaction, Western blotting, immunofluorescence, TUNEL staining, enzyme-linked immunosorbent assays, and immunoprecipitation were applied to examine levels of autophagy flux, ER-stress-induced apoptosis, oxidative stress, and AMPK related signaling pathways. In vitro studies using PC12 cells were performed to discern the relationship between ROS accumulation and autophagy flux blockade. Results: Our results showed that in SCI, defects in autophagy flux contributes to ER stress, leading to neuronal death. Furthermore, SCI enhances the production of reactive oxygen species (ROS) that induce lysosomal dysfunction to impair autophagy flux. We also showed that TFE3 levels are inversely correlated with ROS levels, and increased TFE3 levels can lead to improved outcomes. Finally, we showed that activation of TFE3 after SCI is partly regulated by AMPK-mTOR and AMPK-SKP2-CARM1 signaling pathways. Conclusions: TFE3 is an important regulator in ROS-mediated autophagy dysfunction following SCI, and TFE3 may serve as a promising target for developing treatments for SCI.

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Section: Resultsmentioning

confidence: 99%

TFE3, a potential therapeutic target for Spinal Cord Injury via augmenting autophagy flux and alleviating ER stress

Zhou

Zheng

et al. 2020

Theranostics

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“…It has been shown that t-BHP can cause endothelial cell injury through different pathways [27,28]. To establish the model for endothelial injury, we used t-BHP to induce cell injury in this study.…”

Section: Discussionmentioning

confidence: 99%

Carnosol as a Nrf2 Activator Improves Endothelial Barrier Function Through Antioxidative Mechanisms

Zhang

Hou

et al. 2019

IJMS

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Oxidative stress is the main pathogenesis of diabetic microangiopathy, which can cause microvascular endothelial cell damage and destroy vascular barrier. In this study, it is found that carnosol protects human microvascular endothelial cells (HMVEC) through antioxidative mechanisms. First, we measured the antioxidant activity of carnosol. We showed that carnosol pretreatment suppressed tert-butyl hydroperoxide (t-BHP)-induced cell viability, affected the production of lactate dehydrogenase (LDH) as well as reactive oxygen species (ROS), and increased the produce of nitric oxide (NO). Additionally, carnosol promotes the protein expression of vascular endothelial cadherin (VE-cadherin) to keep the integrity of intercellular junctions, which indicated that it protected microvascular barrier in oxidative stress. Meanwhile, we investigated that carnosol can interrupt Nrf2-Keap1 protein−protein interaction and stimulated antioxidant-responsive element (ARE)-driven luciferase activity in vitro. Mechanistically, we showed that carnosol promotes the expression of heme oxygenase 1(HO-1) and nuclear factor-erythroid 2 related factor 2(Nrf2). It can also promote the expression of endothelial nitric oxide synthase (eNOS). Collectively, our data support the notion that carnosol is a protective agent in HMVECs and has the potential for therapeutic use in the treatments of microvascular endothelial cell injury.

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Ability of Indian pennywort Bacopa monnieri (L.) Pennell in the phytoremediation of sewage (greywater)

Tabassum-Abbasi

Patnaik

Abbasi

2019

Environ Sci Pollut Res

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Attenuation of cytotoxicity induced by tBHP in H9C2 cells by Bacopa monniera and Bacoside A

Cited by 13 publications

References 32 publications

TFE3, a potential therapeutic target for Spinal Cord Injury via augmenting autophagy flux and alleviating ER stress

TFE3, a potential therapeutic target for Spinal Cord Injury via augmenting autophagy flux and alleviating ER stress

Carnosol as a Nrf2 Activator Improves Endothelial Barrier Function Through Antioxidative Mechanisms

Ability of Indian pennywort Bacopa monnieri (L.) Pennell in the phytoremediation of sewage (greywater)

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