Sasanquasaponin-induced cardioprotection involves inhibition of mPTP opening via attenuating intracellular chloride accumulation

Li, Yuanyuan; Xiao, Lin; Qiu, Lingyu; Yan, Yu‐Feng; Wang, Huan; Duan, Guang-Ling; Liao, Zhangping; Chen, Heping

doi:10.1016/j.fitote.2016.11.003

Cited by 10 publications

(9 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The loading of Co 2+ can quench the intracellular fluorescence of calcein except that in mitochondria, for Co 2+ cannot enter mitochondria. Therefore, when mPTP opens, the fluorescence of calcein in mitochondria will be quenched by Co 2+ (21). The PC12 cells were pre-treated as above, and washed with PBS for three times.…”

Section: Mitochondrial Permeability Transition Pore (Mptp) Openingmentioning

confidence: 99%

Thevetiaflavone from Wikstroemia indica ameliorates PC12 cells injury induced by OGD/R via improving ROS-mediated mitochondrial dysfunction

Yao

Yuan

Wei

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Cerebral ischemia and following reperfusion affects many people worldwide. To discover efficient therapeutic approaches, numerous natural products have been investigated. The current study investigated the protective effects of thevetiaflavone, a natural flavonoid obtained from Wikstroemia indica, and the associated mechanisms using PC12 cells induced by oxygen and glucose deprivation. As a result, thevetiaflavone improves cell viability and suppresses the leakage of lactate dehydrogenase from the cytoplasm. Further investigation of the mechanisms demonstrated that thevetiaflavone decreases overproduction of ROS and ameliorates ROS‑mediated mitochondrial dysfunction, including collapse of mitochondrial membrane potential and mitochondrial permeability transition pore opening. Thevetiaflavone reduces the intracellular Ca2+ level, which is closely associated with mitochondrial function and interplays with ROS. Furthermore, thevetiaflavone inhibits apoptosis in PC12 cells through upregulating the expression of Bcl‑2 and downregulating that of Bax and caspase‑3 in addition to increasing the activity of caspase‑3. These results further indicate the protective effects of thevetiaflavone in vivo and its application in the clinic.

show abstract

Section: Mitochondrial Permeability Transition Pore (Mptp) Openingmentioning

confidence: 99%

Thevetiaflavone from Wikstroemia indica ameliorates PC12 cells injury induced by OGD/R via improving ROS-mediated mitochondrial dysfunction

Yao

Yuan

Wei

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…When mPTP is turned on, free solutes and proteins can be distributed in the mitochondrial inner membrane, causing MMP to collapse (Kroemer, 1999). The opening of mPTP causes mitochondrial dysfunction, leading to ATP depletion and ultimately to cardiomyocyte apoptosis (Li et al., 2017; Whelan et al., 2010). Therefore, H/R‐induced mitochondrial dysfunction can be improved by inhibiting [Ca 2+ ] i overload, preventing the excessive production of ROS, blocking the opening of mPTP, increasing MMP, and reducing ATP consumption.…”

Section: Discussionmentioning

confidence: 99%

10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway

Zheng

et al. 2021

Food Science & Nutrition

View full text Add to dashboard Cite

10‐Gingerol (10‐Gin), an active ingredient extracted from ginger, has been reported to have beneficial effects on the cardiovascular system. However, 10‐Gin has not been proved to offer protection against cardiomyocyte injury induced by hypoxia/reoxygenation (H/R). This study aimed to investigate the protective effects of 10‐Gin against H/R‐induced injury and its potential mechanisms in cardiomyocytes. A H/R injury model of H9c2 cardiomyocytes was established using 600 μmol/L CoCl2 to induce hypoxia in the cells for 24 hr and then reoxygenated for 3 hr. 10‐Gin was pretreated with H9c2 cardiomyocytes for 24 hr to assess its cardiomyocyte protection. Our results showed that 10‐Gin improved the viability of H9c2 cardiomyocytes in the H/R model and decreased the activities of creatine kinase, lactate dehydrogenase, and the generation of reactive oxygen species. By intracellular Ca2+ ([Ca2+]i) fluorescence, we found that 10‐Gin could significantly reduce the [Ca2+]i concentration. 10‐Gin administration increased the activities of antioxidase and reduced malondialdehyde content and inflammatory cytokine levels. 10‐Gin also reduced the apoptosis levels. Importantly, 10‐Gin administration decreased the gene and protein expressions of Wnt5a and Frizzled‐2. In conclusion, 10‐Gin alleviates H/R‐induced cardiomyocyte injury, which is associated with the antioxidation, anti‐inflammation, antiapoptosis action, and reduction of [Ca2+]i overload by suppressing the Wnt5a/Frizzled‐2 pathway.

show abstract

“…CCEs are compounds obtained from Camellia cake. CCEs were shown to have cardioprotective and neuroprotective effects in animal experiments (20)(21)(22). Moreover, CCEs were also reported to have potential antimicrobial and anti-cancer effects (11,23,24).…”

Section: Discussionmentioning

confidence: 99%

Camellia cake extracts reduce burn injury through suppressing inflammatory responses and enhancing collagen synthesis

Liu

Xiao

et al. 2020

Food & Nutrition Research

View full text Add to dashboard Cite

Sasanquasaponin-induced cardioprotection involves inhibition of mPTP opening via attenuating intracellular chloride accumulation

Cited by 10 publications

References 32 publications

Thevetiaflavone from Wikstroemia indica ameliorates PC12 cells injury induced by OGD/R via improving ROS-mediated mitochondrial dysfunction

Thevetiaflavone from Wikstroemia indica ameliorates PC12 cells injury induced by OGD/R via improving ROS-mediated mitochondrial dysfunction

10‐Gingerol alleviates hypoxia/reoxygenation‐induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled‐2 pathway

Camellia cake extracts reduce burn injury through suppressing inflammatory responses and enhancing collagen synthesis

Contact Info

Product

Resources

About