Hepatoprotective activity of <i>Terminalia catappa</i> L. leaves and its two triterpenoids

Gao, Jing; Tang, Xin; Dou, Huan; Fan, Yida; Zhao, Xiaoning; Xu, Qiang

doi:10.1211/0022357044733

Cited by 71 publications

(47 citation statements)

References 25 publications

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“…Pretreatment with AA reduced ROS levels in Glu-injured cells (Figure 3). These results are consistent with those of our previous study, which showed that AA has hydroxyl radical-scavenging activity in cell-free systems [40] . The disruption of the MMP may lead to cytochrome c release and activation of caspases that may lead to cell death.…”

Section: Discussionsupporting

confidence: 94%

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

et al. 2012

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Aim: To investigate whether asiatic acid (AA), a pentacyclic triterpene in Centella asiatica, exerted neuroprotective effects in vitro and in vivo, and to determine the underlying mechanisms. Methods: human neuroblastoma Sh-SY5Y cells were used for in vitro study. Cell viability was determined with the MTT assay. hoechst 33342 staining and flow cytometry were used to examine the apoptosis. The mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were measured using fluorescent dye. PGC-1α and Sirt1 levels were examined using Western blotting. Neonatal mice were given monosodium glutamate (2.5 mg/g) subcutaneously at the neck from postnatal day (PD) 7 to 13, and orally administered with AA on PD 14 daily for 30 d. The learning and memory of the mice were evaluated with the Morris water maze test. hE staining was used to analyze the pyramidal layer structure in the CA1 and CA3 regions. Results: Pretreatment of Sh-SY5Y cells with AA (0.1-100 nmol/L) attenuated toxicity induced by 10 mmol/L glutamate in a concentration-dependent manner. AA 10 nmol/L significantly decreased apoptotic cell death and reduced reactive oxygen species (ROS), stabilized the mitochondrial membrane potential (MMP), and promoted the expression of PGC-1α and Sirt1. In the mice models, oral administration of AA (100 mg/kg) significantly attenuated cognitive deficits in the Morris water maze test, and restored lipid peroxidation and glutathione and the activity of SOD in the hippocampus and cortex to the control levels. AA (50 and 100 mg/kg) also attenuated neuronal damage of the pyramidal layer in the CA1 and CA3 regions. Conclusion: AA attenuates glutamate-induced cognitive deficits of mice and protects SH-SY5Y cells against glutamate-induced apoptosis in vitro.

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Section: Discussionsupporting

confidence: 94%

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

et al. 2012

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“…The AA neuroprotective effect was also confirmed with the H 2 O 2 -induced damage. It is consistent with our previous study that AA has hydroxyl radicals scavenging activity [41] . The concentration of AA is critical for its neuroprotection.…”

Section: Discussionsupporting

confidence: 94%

Protective Effects of Asiatic Acid on Rotenone- or H2O2-Induced Injury in SH-SY5Y Cells

Xiong

Ding

et al. 2008

Neurochem Res

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Parkinson's disease (PD) is a progressive neurodegenerative disorder with a prevalence of 1-2% in people over the age of 50. Mitochondrial dysfunction occurred in PD patients showing a 15-30% loss of activity in complex I. Asiatic acid (AA), a triterpenoid, is an antioxidant and used for depression treatment, but the effect of AA against PD-like damage has never been reported. In the present study, we investigated the protective effects of AA against H(2)O(2) or rotenone-induced cellular injury and mitochondrial dysfunction in SH-SY5Y cells. Mitochondrial membrane potential (MMP) and the expression of voltage-dependent anion channel (VDAC) were detected with or without AA pretreatment following cellular injury to address the possible mechanisms of AA neuroprotection. The results showed that pre-treatment of AA (0.01-100 nM) protected cells against the toxicity induced by rotenone or H(2)O(2). In addition, MMP dissipation occurred following the exposure of rotenone, which could be prevented by AA treatment. More interestingly, pre-administration of AA inhibited the elevation of VDAC mRNA and protein levels induced by rotenone(100 nM) or H(2)O(2) (300 microM).These data indicate that AA could protect neuronal cells against mitochondrial dysfunctional injury and suggest that AA might be developed as an agent for PD prevention or therapy.

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“…In our study, the activities of SOD and GPx were found to be decreased in the liver mitochondria of D-GalN-induced hepatotoxicity rats, which is probably due to an accumulation of ROS and severe oxidative stress by D-GalN. GSH is a major defence mechanism against oxidative stress within mitochondria [44]. The depletion in the levels of mitochondrial GSH seems to be a major mechanism in inducing an imbalance of mitochondrial function [45].…”

Section: Discussionmentioning

confidence: 46%

“…GSH depletion and/or increased free radical accumulation may lead to the decrease in the levels of ascorbic acid and a-tocopherol in the liver toxicity rats, which was also observed our study. This condition may aggravate the overproduction of mitochondrial ROS [44]. Treatment with carvacrol reversed these changes towards normality.…”

Section: Discussionmentioning

confidence: 97%

Pharmacological effect of carvacrol on d-galactosamine-induced mitochondrial enzymes and DNA damage by single-cell gel electrophoresis

et al. 2011

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The present study aimed at investigating the effect of carvacrol on hepatic mitochondrial enzyme activities and DNA damage in D: -galactosamine (D: -GalN)-induced hepatotoxicity in male albino Wistar rats. The activities of hepatic mitochondrial enzymes such as isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADPH dehydrogenase and cytochrome c oxidase significantly decreased in D: -GalN-hepatotoxic rats, and administration of carvacrol brought these parameters towards normality. In D: -GalN-hepatotoxic rats, the hepatic mitochondrial concentration of thiobarbituric acid reactive substances significantly increased, and administration of carvacrol significantly reduced them towards normality. Furthermore, the activities of enzymatic antioxidants such as superoxide dismutase and glutathione peroxidase and the levels of non-enzymatic antioxidants such as vitamin C, vitamin E and reduced glutathione decreased significantly in the liver mitochondria. Administration of carvacrol returned the enzymatic and non-enzymatic antioxidants towards normality. D: -GalN-hepatotoxic rats had increased DNA damage, which administration of carvacrol significantly decreased. These results suggest that carvacrol has liver mitochondrial antioxidant properties and possesses a defensive effect against mitochondrial enzymes and DNA damage in D: -GalN-induced rats.

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Hepatoprotective activity of Terminalia catappa L. leaves and its two triterpenoids

Cited by 71 publications

References 25 publications

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

Protective Effects of Asiatic Acid on Rotenone- or H2O2-Induced Injury in SH-SY5Y Cells

Pharmacological effect of carvacrol on d-galactosamine-induced mitochondrial enzymes and DNA damage by single-cell gel electrophoresis

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