Protective effect of isoliquiritin against corticosterone-induced neurotoxicity in PC12 cells

Abstract

Isoliquiritin, a flavonoid glycoside compound from licorice, possesses a broad spectrum of pharmacological activities including antioxidant, anti-inflammatory and anti-depression activities. However, the neuroprotective mechanisms of antidepressant effects remain unclear. In this study, the aim was to investigate the cytoprotective efficiency and potential mechanisms of isoliquiritin in corticosterone-damaged PC12 cells. The results of this study showed that pretreatment of PC12 cells with isoliquiritin significantly prevented corticosterone-induced cell apoptosis. In addition, isoliquiritin increased the activity of dismutase (SOD) and catalase (CAT), decreased the contents of reactive oxygen species (ROS) and malondialdehyde (MDA). These findings suggest that isoliquiritin provides protective action against corticosterone-induced cell damage by reducing oxidative stress. Furthermore, pretreatment with isoliquiritin reduced corticosterone-induced mitochondrial dysfunction by preventing mitochondrial membrane potential dissipation. Our findings indicate that isoliquiritin might exert its therapeutic effects via regulating mitochondrial dysfunction. Moreover, isoliquiritin strongly attenuated intracellular calcium ([Ca]i) overload and down-regulation of Bax, caspase-3 and cytochrome C (Cyt-C) protein expression, and up-regulation of Bcl protein expression. In conclusion, isoliquiritin has a cytoprotective effect on corticosterone-induced neurotoxicity in PC12 cells, which may be related to its antioxidant action, inhibition of [Ca]i overload and inhibition of the mitochondrial apoptotic pathway.

Antidepressant-Like and Neuroprotective Effects of Ethanol Extract from the Root Bark of Hibiscus syriacus L.

“…However, pretreatment with HSR attenuated these changes, indicating that HSR induces mitochondrial protection in vitro. It has been demonstrated that corticosterone induces apoptosis through activation of the caspase-3 apoptosis pathway [40]. Our findings indicate that HSR may exert its therapeutic effects by regulating the mitochondrial dysfunction.…”

Protective effects of macamides fromLepidium meyeniiWalp. against corticosterone-induced neurotoxicity in PC12 cells

“…6,7,12,59 Zhou et al suggested a potential mechanism of toxicity by CORT: CORT causes a large increase in the levels of intracellular ROS, decreases MMP, releases cytochrome C, activates caspase-3, and all of this inducing apoptosis. 53 In our experiment, CORT remarkably increased the number of early and late apoptotic cells, whereas the number of apoptotic cells was considerably reduced aer M 18:3 treatment. Moreover, CORT increased the expression levels of cleaved-caspase-3, Bax, cytochrome C, and cleaved-PARP, and decreased the expression level of Bcl-2.…”

“…57,58 Bcl-2 can competitively bind to Bax on the mitochondrial membrane to form a Bcl-2/Bax heterodimer resulting in closing of the MPTPs and preventing the release of proapoptotic factors from mitochondria, thus achieving an antiapoptotic effect. 53 High levels of CORT cause nerve cell apoptosis in vitro and vivo. 6,7,12,59 Zhou et al suggested a potential mechanism of toxicity by CORT: CORT causes a large increase in the levels of intracellular ROS, decreases MMP, releases cytochrome C, activates caspase-3, and all of this inducing apoptosis.…”

Neuroprotective effect of polysaccharides from Gastrodia elata blume against corticosterone‑induced apoptosis in PC12 cells via inhibition of the endoplasmic reticulum stress‑mediated pathway

“…CORT is the major rodent glucocorticoid, and exposure to continued high CORT concentrations can cause lymphocyte, cortex and hippocampal nerve cell damage (12), which can be reversed by antidepressants. There is also sufficient evidence to suggest that a drug possessing the ability to reverse CORT-induced neurotoxicity may have a possible therapeutic potential in preventing or treating major depression (13).…”