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Fang Wang - One of the best experts on this subject based on the ideXlab platform.

  • sulforaphane alleviates ethanol mediated central inhibition and reverses Chronic Stress induced aggravation of acute alcoholism via targeting nrf2 regulated catalase expression
    Neuropharmacology, 2020
    Co-Authors: Yu Cao, Wen Wang, Jianguo Chen, Fang Wang
    Abstract:

    Acute ethanol intoxication by excessive drinking is an important cause of alcohol-induced death. Stress exposure has been identified as one risk factor for alcohol abuse. Previous reports indicated that Stressors may augment inhibitory effects of alcohol, but the underlying mechanism remains unknown. Here, we reported that Chronic Unpredictable Stress increased the sensitivity to the acute ethanol intoxication in mice via impairing nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-catalase signaling. Nrf2 activity regulates the expression of catalase, a key antioxidant enzyme that mediates ethanol oxidation in the brain. Pharmacological blockade of catalase or Nrf2 activity significantly aggravated acute ethanol intoxication. Sulforaphane, a cruciferous vegetable-derived activator of Nrf2, significantly attenuated acute ethanol intoxication. Furthermore, the Stress-induced aggravation of acute alcoholism was rapidly reversed by sulforaphane. Our findings suggest that Nrf2 may function as a novel drug target for the prevention of acute alcoholism, especially in psychiatric patients, by controlling catalase-mediated ethanol oxidation.

  • angiotensin converting enzyme inhibitor rapidly ameliorates depressive type behaviors via bradykinin dependent activation of mammalian target of rapamycin complex 1
    Biological Psychiatry, 2020
    Co-Authors: Han Luo, Tiantian Shen, Ji Wang, Jiangeng Huang, Silong Deng, Lihong Long, Yu Cao, Ming Jin, Qianqian Han, Fang Wang
    Abstract:

    Abstract Background Angiotensin-converting enzyme inhibitors (ACEIs) are widely prescribed antihypertensive agents. Intriguingly, case reports and clinical trials have indicated that ACEIs, including captopril and lisinopril, may have a rapid mood-elevating effect in certain patients, but few experimental studies have investigated their value as fast-onset antidepressants. Methods The present study consisted of a series of experiments using biochemical assays, immunohistochemistry, and behavioral techniques to examine the effect and mechanism of captopril on depressive-like behavior in 2 animal models, the Chronic Unpredictable Stress model and the Chronic social defeat Stress model. Results Captopril (19.5 or 39 mg/kg, intraperitoneal injection) exerted rapid antidepressant activity in mice treated under the Chronic Unpredictable Stress model and mice treated under the Chronic social defeat Stress model. Pharmacokinetic analysis revealed that captopril crossed the blood-brain barrier and that lisinopril, another ACEI with better blood-brain barrier permeability, exerted a faster and longer-lasting effect at a same molar equivalent dose. This antidepressant effect seemed to be independent of the renin-angiotensin system, but dependent on the bradykinin (BK) system, since the decreased BK detected in the Stressed mice could be reversed by captopril. The hypofunction of the downstream effector of BK, Cdc42 (cell division control protein 42) homolog, contributed to the Stress-induced loss of dendritic spines, which was rapidly reversed by captopril via activating the mTORC1 (mammalian target of rapamycin complex 1) pathway. Conclusions Our findings indicate that the BK-dependent activation of mTORC1 may represent a promising mechanism underlying antidepressant pharmacology. Considering their affordability and availability, ACEIs may emerge as a novel fast-onset antidepressant, especially for patients with comorbid depression and hypertension.

  • angiotensin converting enzyme inhibitor rapidly ameliorates depressive type behaviors via bradykinin dependent activation of mammalian target of rapamycin complex 1
    Biological Psychiatry, 2020
    Co-Authors: Pengfei Wu, Tiantian Shen, Ji Wang, Jiangeng Huang, Jingang He, Silong Deng, Lan Ni, Zhuangli Hu, Lihong Long, Fang Wang
    Abstract:

    Abstract Background Angiotensin-converting enzyme inhibitors (ACEIs) are widely prescribed antihypertensive agents. Intriguingly, case reports and clinical trials have indicated that ACEIs, including captopril and lisinopril, may have a rapid mood-elevating effect in certain patients, but few experimental studies have investigated their value as fast-onset antidepressants. Methods The present study consisted of a series of experiments using biochemical assays, immunohistochemistry, and behavioral techniques to examine the effect and mechanism of captopril on depressive-like behavior in 2 animal models, the Chronic Unpredictable Stress model and the Chronic social defeat Stress model. Results Captopril (19.5 or 39 mg/kg, intraperitoneal injection) exerted rapid antidepressant activity in mice treated under the Chronic Unpredictable Stress model and mice treated under the Chronic social defeat Stress model. Pharmacokinetic analysis revealed that captopril crossed the blood-brain barrier and that lisinopril, another ACEI with better blood-brain barrier permeability, exerted a faster and longer-lasting effect at a same molar equivalent dose. This antidepressant effect seemed to be independent of the renin-angiotensin system, but dependent on the bradykinin (BK) system, since the decreased BK detected in the Stressed mice could be reversed by captopril. The hypofunction of the downstream effector of BK, Cdc42 (cell division control protein 42) homolog, contributed to the Stress-induced loss of dendritic spines, which was rapidly reversed by captopril via activating the mTORC1 (mammalian target of rapamycin complex 1) pathway. Conclusions Our findings indicate that the BK-dependent activation of mTORC1 may represent a promising mechanism underlying antidepressant pharmacology. Considering their affordability and availability, ACEIs may emerge as a novel fast-onset antidepressant, especially for patients with comorbid depression and hypertension.

Anil Kumar - One of the best experts on this subject based on the ideXlab platform.

  • Quercetin along with piperine prevents cognitive dysfunction, oxidative Stress and neuro-inflammation associated with mouse model of Chronic Unpredictable Stress
    Archives of Pharmacal Research, 2017
    Co-Authors: Puneet Rinwa, Anil Kumar
    Abstract:

    Stress occurs in everyday life and persistence of it causes memory loss. Bioflavonoids like quercetin are reported to have poor bioavailability and limited therapeutic potential against Stress induced neurological disorders. Therefore, the present study is an attempt to elucidate the therapeutic potency of combination of quercetin with piperine; a bioavailability enhancer against Chronic Unpredictable Stress (CUS)-induced behavioral and biochemical alterations. Laca mice were subjected to a series of Stressful events for a period of 28 days. Quercetin (20, 40 and 80 mg/kg, p.o.), piperine (20 mg/kg, p.o.) and their combinations were administered daily 30 min before CUS procedure. Piracetam (100 mg/kg, i.p.) served as a standard control. CUS caused impaired spatial navigation in Morris water maze test and poor retention in elevated plus maze task. Further, there was significant increase in brain oxidative Stress markers and neuro-inflammation (TNF-α). This was coupled with marked rise in acetylcholinesterase and serum corticosterone levels. Co-administration of piperine with quercetin significantly elevated their potential to restore these behavioral, biochemical and molecular changes associated with mouse model of CUS. These results suggest that piperine enhances the neuroprotective effects of quercetin against CUS-induced oxidative Stress, neuro-inflammation and memory deficits.

  • Modulation of nitrergic signalling pathway by American ginseng attenuates Chronic Unpredictable Stress-induced cognitive impairment, neuroinflammation, and biochemical alterations
    Naunyn-Schmiedeberg's Archives of Pharmacology, 2014
    Co-Authors: Puneet Rinwa, Anil Kumar
    Abstract:

    Prolonged Stress causes extensive loss of neurons leading to deficits in cognitive performance. Increasing evidence indicates that accumulation of intercellular messenger, nitric oxide (NO), plays a crucial role in the pathogenesis of memory disorders. American ginseng (AG) is known to show protection in different animal models of neurological diseases; however, its exact mechanism of action is not clearly understood. Therefore, the current study was designed to investigate the interaction of AG against Chronic Unpredictable Stress (CUS)-associated behavioral and biochemical alterations and the probable role of nitrergic pathway in this effect. Male Laca mice were exposed to a series of Stressors along with drug/vehicle treatment daily for 28 days. CUS paradigm caused significant impairment in both acquisition and retention memory as measured in Morris water maze and elevated plus maze task. This was coupled with alterations in oxidative Stress markers, mitochondrial enzyme complex activities, pro-inflammatory cytokine (TNF-α), and acetylcholinesterase levels in the hippocampus as compared with naïve group. Besides, there was a marked increase in serum corticosterone levels. AG (100, 200 mg/kg; p.o.) treatment significantly improved cognitive impairment; reduced TNF-α, acetylcholinesterase, and corticosterone levels; and attenuated oxidative–nitrergic Stress. Furthermore, pre-treatment of l -arginine (100 mg/kg; i.p.), a nitric oxide donor, with subeffective dose of AG (100 mg/kg; p.o.) reversed its protective effects. However, l -NAME (10 mg/kg, i.p.), a non-specific NO synthase inhibitor, potentiated the effects of AG. Our findings suggest that modulation of nitrergic signalling cascade is involved in the protective effects of AG against CUS-induced cognitive dysfunction, oxidative Stress, and neuroinflammation.

  • piperine potentiates the protective effects of curcumin against Chronic Unpredictable Stress induced cognitive impairment and oxidative damage in mice
    Brain Research, 2012
    Co-Authors: Puneet Rinwa, Anil Kumar
    Abstract:

    Life event Stressors are the major vulnerability factors for the development of cognitive disorders. A vital therapeutic for Stress related disorders is curcumin, derived from curry spice turmeric. Dietary phytochemicals are currently used as an adjuvant therapy to accelerate their therapeutic efficacy. Therefore, the present study was designed to investigate the effect of curcumin and its co-administration with piperine against Chronic Unpredictable Stress (CUS)-induced cognitive impairment and oxidative Stress in mice. Male Laca mice were subjected to undergo a battery of Stressors for a period of 28 days. Vehicle/drugs were administered daily 30mins before CUS procedure. Chronic Stress significantly impaired memory performance (delayed latency time to reach platform in Morris water maze as well as to reach closed arm in elevated plus maze test) and decreased locomotor activity along with sucrose consumption. Further, there was a significant impairment in oxidative parameters (elevated malondialdehyde, nitrite concentration and decreased reduced glutathione, catalase levels) and mitochondrial enzyme complex activities, along with raised acetylcholinesterase and serum corticosterone levels. Chronic treatment with curcumin (200 and 400mg/kg, p.o.) significantly improved these behavioral and biochemical alterations, restored mitochondrial enzyme complex activities and attenuated increased acetylcholinesterase and serum corticosterone levels. In addition, co-administration of piperine (20mg/kg; p.o.) with curcumin (100 and 200mg/kg, p.o.) significantly elevated the protective effect as compared to their effects alone. The results clearly suggest that piperine enhanced the bioavailability of curcumin and potentiated its protective effects against CUS induced cognitive impairment and associated oxidative damage in mice.

Gabriel Nowak - One of the best experts on this subject based on the ideXlab platform.

  • Chronic Unpredictable Stress induced reduction in the hippocampal brain derived neurotrophic factor bdnf gene expression is antagonized by zinc treatment
    Pharmacological Reports, 2011
    Co-Authors: Katarzyna Cieślik, Magdalena Sowakucma, Grazyna Ossowska, Beata Legutko, Malgorzata Wolak, Wlodzimierz Opoka, Gabriel Nowak
    Abstract:

    Preclinical data indicate the antidepressant activity of zinc and the involvement of the brain-derived neurotrophic factor (BDNF) in this mechanism. The present study investigates the effect of Chronic (16 days) combined treatment with zinc (15 mg/kg zinc hydroaspartate) and imipramine (5 mg/kg) in Chronic Unpredictable Stress (CUS) on the BDNF mRNA level in the rat brain. Moreover, serum zinc concentrations were also assessed. CUS induced a significant reduction in the BDNF mRNA level in the hippocampus by 21% but had no effect in the frontal cortex. Repeated treatment with zinc induced a significant increase in the BDNF mRNA level in the hippocampus in the unStressed animals by 12% and as in the Chronically Stressed animals by 14%, compared to the appropriate controls. Imipramine treatment did not affect this factor. However, combined treatment of zinc and imipramine induced a 12% elevation of the BDNF mRNA level in the Stressed but not in the unStressed rats. CUS induced a 19% reduction in the serum zinc concentration, whereas combined treatment of zinc and imipramine reduced this concentration by 24% in the unStressed and increased it (by 20%) in the Stressed animals. These results indicate that: 1) CUS induces a reduction in the BDNF gene expression with a concomitant diminution of serum zinc concentration and 2) the CUS-induced reduction in the BDNF gene expression is antagonized by Chronic treatment with zinc.

Marianne Hald Larsen - One of the best experts on this subject based on the ideXlab platform.

  • regulation of brain derived neurotrophic factor bdnf in the Chronic Unpredictable Stress rat model and the effects of Chronic antidepressant treatment
    Journal of Psychiatric Research, 2010
    Co-Authors: Marianne Hald Larsen, Jens D Mikkelsen, Anders Hayschmidt, Carmen Sandi
    Abstract:

    Chronic Unpredictable Stress (CUS) is a widely used animal model of depression. The present study was undertaken to investigate behavioral, physiological and molecular effects of CUS and/or Chronic antidepressant treatment (venlafaxine or imipramine) in the same set of animals. Anhedonia, a core symptom of depression, was assessed by measuring consumption of a palatable solution. Exposure to CUS reduced intake of a palatable solution and this effect was prevented by Chronic antidepressant treatment. Moreover, Chronic antidepressant treatment decreased depressive-like behavior in a modified forced swim test in Stressed rats. Present evidence suggests a role for brain-derived neurotrophic factor (BDNF) in depression. BDNF mRNA levels in the ventral and dorsal hippocampus were assessed by in situ hybridization. Exposure to CUS was not correlated with a decrease but rather with an increase in BDNF mRNA expression in both the dentate gyrus of the dorsal hippocampus and the CA3 region of the ventral hippocampus indicating that there is no simple link between depression-like behaviors per se and brain BDNF levels in rats. However, a significant increase in BDNF mRNA levels in the dentate gyrus of the dorsal hippocampus correlated with Chronic antidepressant treatment emphasizing a role for BDNF in the mechanisms underlying antidepressant activity.

Jianyou Guo - One of the best experts on this subject based on the ideXlab platform.

  • effect of xingpijieyu decoction on spatial learning and memory and camp pka creb bdnf pathway in rat model of depression through Chronic Unpredictable Stress
    BMC Complementary and Alternative Medicine, 2017
    Co-Authors: Chunye Wang, Jianyou Guo, Rongjuan Guo
    Abstract:

    Depression is a mental disorder characterized by a pervasive low mood and loss of pleasure or interest in usual activities, and often results in cognitive dysfunction. The disturbance of cognitive processes associated with depression, especially the impairment of learning and memory, exacerbates illness and increases recurrence of depression. XingPiJieYu (XPJY) is one of the most widely clinical formulas of traditional Chinese medicine (TCM) and can improve the symptoms of depression, including learning and memory. However, its regulatory effects haven’t been comprehensively studied so far. Recently, some animal tests have indicated that the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA)-cAMP response element-binding protein (CREB)-brain derived neurotrophic factor (BDNF) signaling pathway in hippocampus is closely related to depression and the pathogenesis of cognitive function impairments. The present study was performed to investigate the effect and mechanism of XPJY on depression and learning and memory in animal model. The rat model of depression was established by Chronic Unpredictable Stress (CUS) for 21 days. The rats were randomly divided into six groups: control group, CUS group, CUS + XPJY (1.4 g/kg, 0.7 g/kg and 0.35 g/kg) groups, and CUS + sertraline (10 mg/kg) group. The sucrose preference, open field exploration and Morris water maze (MWM) were tested. The expression of cAMP, CREB, PKA and BDNF protein in hippocampus was examined with Elisa and Western Blot. The mRNA level of CREB and BDNF in hippocampus was measured with PCR. The results demonstrated that rats subjected to CUS exhibited decreases in sucrose preference, total ambulation, percentage of central ambulation, rearing in the open field test and spatial performance in the MWM. CUS reduced the expression of cAMP, PKA, CREB and BDNF in hippocampus of model rats. These effects could be reversed by XPJY. The results indicated that XPJY can improve depression and related learning and memory and the effect of XPJY is partly exerted through the cAMP-PKA-CREB-BDNF signaling pathway.

  • acupuncture ameliorates inflammatory response in a Chronic Unpredictable Stress rat model of depression
    Brain Research Bulletin, 2017
    Co-Authors: Runhui Shao, Shuying Jin, Jianyou Guo
    Abstract:

    Depression is one of the most common psychiatric disorders. Chronic inflammatory response has been viewed as a key factor in depression. Acupuncture in Chinese medicine has been shown to be an effective treatment for depression. In the present study, we investigated the mechanism underlying antidepressant effect of acupuncture. The rats were subjected to Chronic Unpredictable mild Stress (CUMS) for 28days to induce depressive-like behaviors. Acupuncture treatment was applied once every other day during the 28-day Stress period. The behavioral tests (body weight, sucrose consumption and locomotor activity) were performed. The expressions of nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor kappa B (NF-κB) were determined in the rat hippocampus and prefrontal cortex. CUMS induced depressive-like behavior in rats, which was alleviated by acupuncture treatment. The increased levels of NO, PGE2, iNOS and COX-2 induced by CUMS, were all significantly decreased in the hippocampus and prefrontal cortex by acupuncture. Moreover, acupuncture markedly inhibited the activation of NF-κB in rats. These findings showed that the antidepressant-like effect of acupuncture might be mediated by inhibition of inflammatory mediators via modulation of NF-κB in the brain regions.

  • Chronic treatment with celecoxib reverses Chronic Unpredictable Stress induced depressive like behavior via reducing cyclooxygenase 2 expression in rat brain
    European Journal of Pharmacology, 2009
    Co-Authors: Jianyou Guo, Yeping Ruan, Meng Sun, Baosheng Zhao, Fei Luo
    Abstract:

    Recent clinical trails reported that adjunctive cyclooxygenase (COX)-2 inhibition with celecoxib is beneficial in treating depression. However, another clinical study showed celecoxib did not have inhibitory effect of COX-2 in human brain when given at a therapeutic dose. Therefore, whether celecoxib is exerting its influence through COX inhibition or by some other mechanism remains unclear. The present study further investigated the effect of celecoxib on COX-2 expression, prostaglandin E(2) (PGE(2), a major COX-2-mediated inflammatory mediator) concentration and the depressive-like behaviors in rats. Celecoxib was administrated by oral gavage to naive rats (16 mg/kg) or Stressed rats (2, 8, 16 mg/kg, respectively) for 21 days, or to Stressed rats for a single dose (16 mg/kg). The results showed that 21 days Chronic Unpredictable Stress induced depressive-like behaviors and increased the COX-2 expression and PGE(2) concentration in rat brain. Chronic treatments with celecoxib alleviated the depressive-like behavior and reversed the levels of COX-2 expression and PGE2 concentration in Stressed rat in a dose-dependent manner. Celecoxib also improved the emotional state and decreased COX-2 expression and PGE(2) concentration in naive rats. In addition, a single dose of celecoxib treatment reversed COX-2 expression and PGE(2) concentration. but didn't alter the depressive-like behavior in Stressed rat. These results suggest that COX-2 enzyme might play a key role in pathophysiology of depression. Furthermore, these data indicate that Chronic celecoxib treatment reverse Chronic Unpredictable Stress-induced depressive-like behavior might via reducing COX-2 enzyme in brain, and the selective COX-2 inhibitors could be developed as potential remedies for the management of depression. (C) 2009 Elsevier B.V. All rights reserved.