Umbelliferone reverses depression-like behavior in chronic unpredictable mild stress-induced rats by attenuating neuronal apoptosis via regulating ROCK/Akt pathway

Qin, Tingting; Fang, Fang; Song, Meiting; Li, Ruipeng; Ma, Zhigui; Ma, Shengming

doi:10.1016/j.bbr.2016.09.039

Cited by 65 publications

(36 citation statements)

References 48 publications

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“…G-Rg1: ginsenoside-Rg1; FLX: fluoxetine; SPT: sucrose preference test; FST: forced swim test. Continued 6. Oxidative Medicine and Cellular Longevity the nonstressed control group (P > 0:05).…”

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confidence: 93%

“…Recent evidence has indicated that depression is associated with increases in oxidative stress and inflammation, followed by a consequent activation in neuronal apoptosis. Such responses are, in part, due to environmental risk factors which then produce a neuroprogression of events resulting in the development of depression-like behaviors [4][5][6]. Results from clinical reports have shown that inflammation is closely associated with the pathogenesis of depression, as indicated by elevated levels of proinflammatory cytokines found in the peripheral circulation and some brain regions of depressed patients [7,8].…”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside-Rg1 Rescues Stress-Induced Depression-Like Behaviors via Suppression of Oxidative Stress and Neural Inflammation in Rats

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Depression is an inflammatory-related condition, with the progression in neuronal damage resulting in major depression disorder. Ginsenoside-Rg1, a sterol extract from the herb Panax ginseng, has been shown to exert neuroprotective effects upon neurodegeneration disorders. However, whether ginsenoside-Rg1 confers antidepressant-like effects on neuroinflammation as associated with depression, as well as the possible mechanism involved in these neuroprotective effects, is currently unclear. In the present report, we show that treatment with ginsenoside-Rg1 (40 mg/kg, i.p.) significantly ameliorated depressive-like behaviors as induced by chronic unpredictable mild stress (CUMS) in a rat model of depression. Moreover, these CUMS rats treated with ginsenoside-Rg1 showed reductions in the levels of the oxidative stress products and the activity in the antioxidant stress kinase. Furthermore, CUMS rats treated with ginsenoside-Rg1 showed ameliorated neuroinflammation and associated neuronal apoptosis along with a reduction in dendritic spine atrophy and display of depressive behaviors. Taken together, the results of this study suggest that ginsenoside-Rg1 produces antidepressant-like effects in CUMS-exposed rats; and one of the mechanisms for these antidepressant-like effects of ginsenoside-Rg1 appears to involve protection against oxidative stress and thus the neuronal deterioration resulting from inflammatory responses. These findings provide evidence for the therapeutic potential of ginsenoside-Rg1 in the treatment of stress-related depression.

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confidence: 93%

Section: Introductionmentioning

confidence: 99%

Ginsenoside-Rg1 Rescues Stress-Induced Depression-Like Behaviors via Suppression of Oxidative Stress and Neural Inflammation in Rats

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Thus, both the doses of ES‐PE could decrease the immobile time ( n = 6–10). ANOVA, F = 15.81, P < 0.0001. (F) ES‐PE decreased the immobile time prolonged by CUMS in FST ( n = 6–13).…”

Section: Resultsmentioning

confidence: 96%

Extract of Euryale ferox Salisb exerts antidepressant effects and regulates autophagy through the adenosine monophosphate‐activated protein kinase—UNC‐51‐like kinase 1 pathway

Huang

Wang

et al. 2018

IUBMB Life

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Positive regulation of autophagy by Euryale ferox Salisb (ES) leads to antidepressant effects. This study focused on the potential antidepressant mechanisms induced by the petroleum ether fraction of ES (ES-PE) in the chronically unpredictable mild stress (CUMS) mouse model. Deficits in the sucrose preference test, open field test, tail suspension test, and forced swim test were observed following CUMS, and were reversed following ES-PE administration. Contrary to the expression of mammalian target of rapamycin, autophagy was decreased after establishment of the CUMS model. We also observed trends for downregulation of adenosine mononphosphate-activated protein kinase (AMPK) and mammalian autophagy-initiating kinase (ULK1), which were differentially affected by ES-PE. HT22 cells and Compound C, an inhibitor of AMPK, were used to verify the results in mice. Gas chromatography-mass spectrometry analysis revealed high level of vitamin E acetate in ES-PE. Taken together, our data indicate that ES-PE activated autophagy by regulating the AMPK pathway. © 2018 IUBMB Life, 70(4):300-309, 2018.

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“…Umbelliferone (7-hydroxycoumarin) is a simple coumarin found in many plants from the Apiaceae family (Leal, Ferreira, Bezerra, Matos, & Viana, 2000). Umbelliferone reportedly exhibits neuroprotective properties in a chronic unpredictable mild stress-induced rat model of depression (Qin et al, 2017), a rat model of focal cerebral ischaemiareperfusion (Wang, Li, Wang, Fu, & Ma, 2015), and a mouse model of Parkinson's disease (Subramaniam & Ellis, 2013). Additionally, accumulating evidence suggests that umbelliferone activates nuclear factor erythroid-derived 2-like 2 (Nrf2) in various animal models, resulting in upregulation of haem oxygenase-1 (HO-1) and attenuation of excessive inflammatory responses (Hassanein, Mohamed, Shalkami, Khalaf, & Hemeida, 2018;Mahmoud, Germoush, Alotaibi, & Hussein, 2017;Mohamed, Emam, Hassan, & Mogadem, 2014).…”

Section: Introductionmentioning

confidence: 99%

Xanthotoxin and umbelliferone attenuate cognitive dysfunction in a streptozotocin‐induced rat model of sporadic Alzheimer's disease: The role of JAK2/STAT3 and Nrf2/HO‐1 signalling pathway modulation

Hindam

Sayed

Skalicka‐Woźniak

et al. 2020

Phytotherapy Research

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The aim of the present study was to assess the neuroprotective effects of xanthotoxin and umbelliferone in streptozotocin (STZ)‐induced cognitive dysfunction in rats. Animals were injected intracerebroventricularly (ICV) with STZ (3 mg/kg) once to induce a sporadic Alzheimer's disease (SAD)‐like condition. Xanthotoxin or umbelliferone (15 mg/kg, i.p.) were administered 5 hr after ICV‐STZ and daily for 20 consecutive days. Xanthotoxin or umbelliferone prevented cognitive deficits in the Morris water maze and object recognition tests. In parallel, xanthotoxin or umbelliferone reduced hippocampal acetylcholinestrase activity and malondialdehyde level. Moreover, xanthotoxin or umbelliferone increased glutathione content. These coumarins also modulated neuronal cell death by reducing the level of proinflammatory cytokines (tumour necrosis factor‐alpha and interleukin‐6), inhibiting the overexpression of inflammatory markers (nuclear factor κB [NF‐κB] and cyclooxygenase II), and upregulating the expression of NF‐κB inhibitor (IκB‐α). Interestingly, xanthotoxin diminished phosphorylated JAK2 and phosphorylated STAT3 protein expression, while umbelliferone markedly replenished nuclear factor erythroid‐derived 2‐like 2 (Nrf2) and haem oxygenase‐1 (HO‐1) levels. The current study provides evidence for the protective effect of xanthotoxin and umbelliferone in STZ‐induced cognitive dysfunction in rats. This effect may be attributed, at least in part, to inhibiting acetylcholinestrase and attenuating oxidative stress, neuroinflammation and neuronal loss.

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Umbelliferone reverses depression-like behavior in chronic unpredictable mild stress-induced rats by attenuating neuronal apoptosis via regulating ROCK/Akt pathway

Cited by 65 publications

References 48 publications

Ginsenoside-Rg1 Rescues Stress-Induced Depression-Like Behaviors via Suppression of Oxidative Stress and Neural Inflammation in Rats

Ginsenoside-Rg1 Rescues Stress-Induced Depression-Like Behaviors via Suppression of Oxidative Stress and Neural Inflammation in Rats

Extract of Euryale ferox Salisb exerts antidepressant effects and regulates autophagy through the adenosine monophosphate‐activated protein kinase—UNC‐51‐like kinase 1 pathway

Xanthotoxin and umbelliferone attenuate cognitive dysfunction in a streptozotocin‐induced rat model of sporadic Alzheimer's disease: The role of JAK2/STAT3 and Nrf2/HO‐1 signalling pathway modulation

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