scholarly journals Influence of miR-1 on Nerve Cell Apoptosis in Rats with Cerebral Stroke via Regulating ERK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yuanding Jiang ◽  
Tao Wang ◽  
Jian He ◽  
Quan Liao ◽  
Jingjing Wang
Keyword(s):  
Infarct Size ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Sham Group ◽  
Cerebral Infarct ◽  
Erk Signaling ◽  
Model Group ◽  
Protein Levels ◽  
The Brain ◽  
Brain Tissues

To explore the effect of miR-1 on neuronal apoptosis in rats with stroke through the ERK signaling pathway. Methods. Forty male rats (180-220 g) were selected and randomly divided into the sham, model, miR-1 inhibitor, and miR-1 mimic groups (10 rats per group) by average body weight. Cerebral ischemia/reperfusion (I/R) models were established using a modified middle cerebral artery wire thrombosis (MCAO) method in rats in the model group, miR-1 inhibitor group, and miR-1 mimic group. After the successful model establishment, the miR-1inhibitor group and miR-1 mimic group were intravenously injected with miR-1 inhibitor and miR-1 mimic, respectively, once a day for 3 days. The sham and model groups were given the same dose of normal saline. TTC staining was applied to detect the cerebral infarct size and calculate the infarct volume. Histopathological changes in the hippocampus of rat brains were observed by HE staining. Flow cytometry was used to detect neuronal apoptosis in rat brains. The mRNA expressions of miR-1, ERK1/2, Bcl-2, and Bax in rat brain tissues were determined by QRT PCR, and the protein levels of ERK1/2, Bcl-2, Bax, and caspase-3 were determined by Western blot analysis. Results. Compared with the sham group, the neurological impairment score, cerebral infarct size, and volume of rats in the model group were significantly increased ( p < 0.05 ). Compared with the model group, the neurological impairment score, cerebral infarct size, and volume were significantly increased in the miR-1 mimic group and significantly decreased in the miR-1 inhibitor group ( p < 0.05 ). In the model group, the hippocampal tissue of rats had malaligned cells, neuron cell atrophy became smaller, the intercellular spaces became larger, and vacuoles appeared. Compared with the model group, the miR-1 inhibitor group could effectively alleviate the pathological changes in the hippocampus, and the miR-1 mimic group could significantly add to the pathological changes in the rat hippocampus. Compared with the sham group, the mRNA expression of miR-1 and Bax in the brain of model rats increased significantly ( p < 0.05 ), and the mRNA expression of ERK1/2 decreased significantly; Compared with the model group, the miR-1 and Bax mRNA expressions in the brain tissues of rats in the miR-1 inhibitor group were significantly decreased, the ERK1/2 and bcl-2 mRNA expressions were significantly increased, and the miR-1 and Bax mRNA expressions in the brain tissues of rats in the miR-1 inhibitor group were significantly decreased, and the Bcl-2 mRNA expression was significantly increased ( p < 0.05 ). Compared with the sham group, neuronal apoptosis was increased in the brain tissues of rats in the model group and miR-1 mimic group. Compared with the model group, neuronal apoptosis was decreased in the brain tissues of rats in the miR-1 inhibitor group. Compared with the sham group, the ERK1/2 proteins in the model group were significantly decreased, the Bcl-2, Bax, and caspase-3 proteins were significantly increased, and the ERK1/2, Bcl-2, Bax, and caspase-3 proteins in the miR-1 inhibitor group and miR-1 mimic group were significantly increased. Compared with the model group, the protein levels of ERK1/2 and Bcl-2 in the miR-1 inhibitor group were significantly increased, the proteins of Bax and caspase-3 were significantly decreased, and the protein levels of ERK1/2 and Bcl-2 in the miR-1 inhibitor group were significantly increased ( p < 0.05 ). Conclusions. miR-1 can interfere with neuronal apoptosis in rats with stroke through the ERK signaling pathway.

scholarly journals Neuroprotective Effects of Danshen Chuanxiongqin Injection Against Ischemic Stroke: Metabolomic Insights by UHPLC-Q-Orbitrap HRMS Analysis

2021 ◽  
Vol 8 ◽  
Author(s):  
Peipei Zhou ◽  
Lin Zhou ◽  
Yingying Shi ◽  
Zhuolun Li ◽  
Liwei Liu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Infarct Size ◽  
Brain Tissue ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Cerebral Infarct ◽  
Sphingolipid Metabolism ◽  
Neuroprotective Effects ◽  
Behavioral Abnormality

The incidence of cerebral ischemic stroke characterized by high mortality is increasing every year. Danshen Chuanxiongqin Injection (DSCXQ), a traditional Chinese medicine (TCM) preparation, is often applied to treat cerebral apoplexy and its related sequelae. However, there is a lack of systematic research on how DSCXQ mediates its protective effects against cerebral ischemia stroke. Metabolomic analysis based on UHPLC-Q-Orbitrap HRMS was employed to explore the potential mechanisms of DSCXQ on ischemic stroke induced by transient middle cerebral artery occlusion (MCAO). Pattern analysis and metabolomic profiling, combined by multivariate analysis disclosed that 55 differential metabolites were identified between Sham group and Model group, involving sphingolipid metabolism, glycerophospholipid metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, primary bile acid biosynthesis, pantothenate and CoA synthesis and valine, leucine and isoleucine biosynthesis pathways. DSCXQ could reverse brain metabolic deviations in stroke by significantly upregulating the levels of L-tryptophan, Lyso (18:0/0:0), LPC (18:2), Indole-3-methyl acetate, and downregulating the levels of sphinganine 1-phosphate, L-threonic acid, glutaconic acid and N6,N6,N6-Trimethyl-L-lysine. In our study, we focused on the neuroprotective effects of DSCXQ against neuroinflammatory responses and neuronal apoptosis on a stroke model based on sphingolipid metabolism. The expressions of Sphk1, S1PR1, CD62P, Bcl-2, Bax, and cleaved Caspase-3 in brain tissue were evaluated. The neurological deficit, cerebral infarct size and behavioral abnormality were estimated. Results showed that DSCXQ intervention significantly reduced cerebral infarct size, ameliorated behavioral abnormality, inhibited the expression of Sphk1, S1PR1, CD62P, Bax, Cleaved Caspase-3, while increased the level of Bcl-2, and prevented neuronal apoptosis. The limitations are that our study mainly focused on the verification of sphingolipid metabolism pathway in stroke, and while other metabolic pathways left unverified. Our study indicates that SphK1-SIP axis may potentiate neuroinflammatory responses and mediate brain damage through neuronal apoptosis, and DSCXQ could suppress the activity of SphK1-SIP axis to protect brain tissue in cerebral ischemia. In conclusion, this study facilitates our understanding of metabolic changes in ischemia stroke and the underlying mechanisms related to the clinical application of DSCXQ.

scholarly journals Glutathione Suppresses Cerebral Infarct Volume and Cell Death after Ischemic Injury: Involvement of FOXO3 Inactivation and Bcl2 Expression

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Juhyun Song ◽  
Joohyun Park ◽  
Yumi Oh ◽  
Jong Eun Lee
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Cerebral Infarction ◽  
Infarct Size ◽  
Cell Survival ◽  
Ischemia Reperfusion ◽  
Ischemic Injury ◽  
Cerebral Infarct ◽  
Ros Scavenging ◽  
The Brain

Ischemic stroke interrupts the flow of blood to the brain and subsequently results in cerebral infarction and neuronal cell death, leading to severe pathophysiology. Glutathione (GSH) is an antioxidant with cellular protective functions, including reactive oxygen species (ROS) scavenging in the brain. In addition, GSH is involved in various cellular survival pathways in response to oxidative stress. In the present study, we examined whether GSH reduces cerebral infarct size after middle cerebral artery occlusionin vivoand the signaling mechanisms involved in the promotion of cell survival after GSH treatment under ischemia/reperfusion conditionsin vitro. To determine whether GSH reduces the extent of cerebral infarction, cell death after ischemia, and reperfusion injury, we measured infarct size in ischemic brain tissue and the expression of claudin-5 associated with brain infarct formation. We also examined activation of the PI3K/Akt pathway, inactivation of FOXO3, and expression of Bcl2 to assess the role of GSH in promoting cell survival in response to ischemic injury. Based on our results, we suggest that GSH might improve the pathogenesis of ischemic stroke by attenuating cerebral infarction and cell death.

scholarly journals Sphingomyelin Synthase 2 Participate in the Regulation of Sperm Motility and Apoptosis

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4231
Author(s):  
Xiatian Li ◽  
Tao Luo ◽  
Hua Li ◽  
Nianlong Yan
Keyword(s):  
Signaling Pathways ◽  
Sperm Motility ◽  
Acrosome Reaction ◽  
Caspase 3 ◽  
Human Sperm ◽  
Erk Signaling ◽  
Sperm Function ◽  
Sphingomyelin Synthase ◽  
Protein Levels ◽  
Penetration Ability

Sphingomylin participates in sperm function in animals, and also regulates the Akt and ERK signaling pathways, both of which are associated with the asthenospermia. Sphingomyelin synthase 2 (SMS2) is involved in the biosynthesis of sphingomylin. To determine the relationship between SMS2 and human sperm function, we analyzed the distribution of SMS2 in human sperm and testes, and SMS2 expression in patients with asthenospermia and normozoospermia; human sperm were treated with anti-SMS2, and the sperm motility, penetration ability into methylcellulose, capacitation and acrosome reaction, and sperm [Ca2+]i imaging were evaluated, while the Akt and ERK pathway and cleaved caspase 3 were also analyzed. Results showed that SMS2 was localized in the testis and human sperm, and the protein levels of normozoospermia were higher than asthenospermia. Inhibition of SMS2 activity significantly decreased sperm motility and penetration ability into methylcellulose, but had no influence on capacitation and acrosome reaction, or on intracellular [Ca2+]i compared to IgG-treated control groups. Moreover, the phosphorylation level of Akt was decreased, whereas the phosphorylation of ERK and cleaved-caspase 3 levels were significantly increased. Taken together, SMS2 can affect sperm motility and penetration ability into methylcellulose, and participate in apoptosis associated with the Akt and ERK signaling pathways.

scholarly journals LuQi Formula Regulates NLRP3 Inflammasome to Relieve Myocardial-Infarction-Induced Cardiac Remodeling in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Xiaoqing Zhang ◽  
Dandan Zhao ◽  
Jiling Feng ◽  
Xiaoli Yang ◽  
Zhenzhen Lan ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Caspase 3 ◽  
Sham Group ◽  
Ventricular Remodeling ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Myocardial Tissue ◽  
Internal Diameter ◽  
Model Group ◽  
Caspase 1

Background. Excessive activation of the nod-like receptor family pyrin domain containing 3(NLRP3) inflammasome plays a significant role in the progression of cardiac injury. In China, it has been well recognized that Chinese herbal medicine is markedly effective in treating cardiovascular diseases (CVDs). LuQi Formula (LQF) has been used clinically for more than 10 years and confirmed to be effective in improving cardiac function and inhibiting apoptosis. However, the specific mechanisms underlying its efficacy are mostly unknown. This study aimed to evaluate whether LQF could alleviate cardiac injury and apoptosis by regulating the NLRP3 inflammasome and the caspase-3/Bax pathway. Purpose. In this study, we investigated the effects of LQF on cardiac remodeling in a mouse model of myocardial infarction (MI) in vivo. Methods. Forty male C57BL/6 mice were randomly divided into four groups: the sham group, the model group, the LQF group, and the perindopril group, with a sample size (n) of 10 mice in each group. Except the sham group, the other groups received left anterior descending (LAD) coronary artery ligation to induce MI and then treated with LQF, perindopril, or saline. Six weeks after MI, echocardiography was used to evaluate cardiac structure and function. Myocardial tissue morphology was observed by haematoxylin and eosin (H&E) staining, and heart samples were stained with Masson’s trichrome to analyse myocardial fibrosis. Myocardial hypertrophy was observed by fluorescent wheat germ agglutinin (WGA) staining. The expressions of NLRP3, ASC, Cle-caspase-1, IL-1β, TXNIP, Cle-caspase-3, Bcl-2, and Bax in heart tissues were assessed by western blot analysis. mRNA expressions of ANP and BNP in heart tissues were measured by RT-PCR. The expression of reactive oxygen species in myocardial tissue was detected by using a DCFH-DA probe. Results. Echocardiographic analysis showed that compared with the model group, the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) in the LQF and perindopril group were increased ( P < 0.05 ), left ventricular internal diameter end diastole (LVIDd) and left ventricular internal diameter end-systole (LVIDs) were reduced ( P < 0.05 ), and H&E and Masson’s trichrome staining of cardiac tissues showed that LQF and perindopril could partially reverse ventricular remodeling and alleviate myocardial fibrosis ( P < 0.05 ). WGA fluorescence results showed that compared with the model group, myocardial hypertrophy was significantly reduced in the LQF and perindopril group. We also found that LQF and perindopril reduce the oxidative stress response in the heart of MI mice. The protein expression of NLRP3, ASC, Cle-caspase-1, IL-1β, TXNIP, Cle-caspase-3, and Bax was downregulated in the LHF and perindopril treatment group, and Bcl-2 expression was upregulated. Conclusion. LQF and perindopril significantly attenuated cardiac injury and apoptosis in the MI model. In addition, we found that LQF effectively inhibited the activation of the NLRP3/ASC/caspase-1/IL-1β cascade, decreased inflammatory infiltration, delayed ventricular remodeling, and downregulated caspase-3/Bax signaling, which can effectively reduce the apoptosis of cardiomyocytes. Perindopril showed the same mechanism.

A mink (Neovison vison) model of self injury: effects of CBP-CREB axis on nerve injury and behavior

2020 ◽  
Author(s):  
Chunxiao Liu ◽  
Xiaolan Guo ◽  
Huazhe Si ◽  
Guangyu Li
Keyword(s):  
Nerve Damage ◽  
Neovison Vison ◽  
Night Vision ◽  
Mechanism Analysis ◽  
Protein Levels ◽  
Self Injury ◽  
Clinical Disorders ◽  
And Behavior ◽  
The Brain ◽  
Brain Tissues

Abstract BackgroundSelf-injurious behavior (SIB) is a clinically challenging problem within both the general population and several clinical disorders. However, the precise molecular mechanism of SIB is still confused, and few animal models exist. Here, we systematic investigated the genesis and development of SIB based on behavioral and pathophysiology study in mink (Neovison vison) models.MethodWe used night-vision video to observe the mink behavior for four weeks,HE stain was performed to characteristic the pathology change of brain. We performed IHC assay to detect the protein level of Iba-1、p-CREB 、CBP and p300 in the brain tissues. Elisa assay used to examined the levels of NfL and NfH in serum and CSF of mink. qRT-PCR assay was mused to detected the expression of Bcl2, NOR1, FoxO4、c-FOS、CBP and p300 in brain tissues. Western blot was used to detect the protein levels of p-CREB、CBP and p300 in brain tissues. We also used Evans Blue as a tracer to detect whether the blood brain barrier was impaired in the brain of mink.RusultFirst we combine behavioral testing, histopathological and molecular biology experiments found that CBP was related with SIB. Mechanism analysis showed that the dysregulation of CBP in brain activated CREB signaling, resulting in nerve damage of brain and SIB symptoms in minks. Importantly, the CBP-CREB interaction inhibitor helped to relieve SIB and nerve damage in brain tissues.ConclusionOur results illustrate an induction of CBP and an activation of CREB, as a novel mechanism in the genesis of SIB. These finding indicate that CBP-CREB axis is critical for SIB and demonstrate the efficacy of the CBP-CREB interaction inhibitor in treating these behaviors.

scholarly journals Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Feng Liang ◽  
Xin Fu ◽  
Yunpengfei Li ◽  
Fanglei Han
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Protein Expression ◽  
Protective Effect ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Neuronal Injury ◽  
Cyclin B1 ◽  
The Brain ◽  
And Oxidative Stress

Abstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., for 21 days after ISF exposure. The protective effect of DOP was estimated by assessing cognitive function using the neurological score and the Morris water maze. Neuronal apoptosis was assessed in the hippocampus using the TUNEL assay, and protein expression of caspase-3, Bax, and Bcl-2 was measured by Western blotting. The levels of cytokines and oxidative stress parameters were assessed by ELISA. Western blotting and RT-PCR were performed to measure the expression of NF-kB, TLR-4, Sirt-1, and cyclin B1 protein in the brain. The cognitive function and neurological function scores were improved in the DOP group compared with the ISF group. Moreover, DOP treatment reduced the number of TUNEL-positive cells and the expression of caspase-3, Bax, and Bcl-2 protein in the brains of rats with neuronal injury. The levels of mediators of inflammation and oxidative stress were reduced in the brain tissue of the DOP group. Treatment with DOP attenuated the protein expression of TLR-4, NF-kB, cyclin B1, and Sirt-1 in the brain tissue of rats with neuronal injury. In conclusion, DOP ameliorates neuronal apoptosis and improves cognitive function in rats with ISF-induced neuronal injury. Moreover, DOP treatment can prevent neuronal injury by regulating the TLR-4/cyclin B1/Sirt-1 pathway.

Abstract 16: Spatiotemporally-Controlled Ultrasound-Triggered Release of Nitric Oxide Using Nano Au-Polymersomes/S-Nitrosoglutathione Mitigates Post-Resuscitation Cerebral Vasoconstriction and Neuronal Apoptosis via Reciprocating Akt-eNOS-NO Signaling

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Wei-Tien Chang ◽  
Woan-Yi Wang ◽  
Min-Hsuan Hsu ◽  
Po-Tsung Kao ◽  
Chih-Hung Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Brain Perfusion ◽  
Tissue Perfusion ◽  
Triggered Release ◽  
Cerebral Vasoconstriction ◽  
No Release ◽  
No Signaling ◽  
The Brain

Introduction: Cerebral vasoconstriction in the post-resuscitation phase worsens neurological outcome. Nitric oxide (NO) plays important roles mediating vasodilatation and anti-apoptotic protection. We therefore designed an Au-polymersomes/S-nitrosoglutathione (Au-PLGA/GSNO) nanoparticle that can be triggered by ultrasound (US) to release NO, and investigated its roles in mitigating cerebral vasoconstriction and neuronal apoptosis post-CPR. Hypothesis: Spatiotemporally controlled, US-triggered NO release by Au-PLGA/GSNO improves post-CPR cerebral perfusion and confers anti-apoptotic neuroprotection. Methods: Using an established rat model of asphyxia cardiac arrest and CPR, Au-PLGA/GSNO (7500 PPM, 0.4 ml) was infused with simultaneous US (1 MHz) stimulation at the brain 10 min after ROSC. Brain tissue perfusion was continuously recorded by OxyFLO probe and cerebral vasculature videoed by CytoCam. The blood was sampled 2 h post-CPR for measurement of nitrate/nitrite, and the brain harvested for measurement of casepase-3, endothelial NO synthase (eNOS) and protein kinase B (Akt). In a subgroup the brain was harvested at 24 h for TUNEL stain. Results: After CPR, marked cerebral vasoconstriction was noted on CytoCam while brain perfusion significantly reduced to ~0.5 folds that of baseline. After Au-PLGA/GSNO infusion and US stimulation, cerebral vasoconstriction was ameliorated and the brain perfusion significantly enhanced ( P < 0.05 vs. CPR control). The plasma NO indicated by nitrate/nitrite 2 h post-CPR was significantly increased ( P < 0.01) while cleaved caspase-3/caspase-3 of the brain markedly reduced ( P < 0.001). TUNEL stain of the hippocampus CA1 and CA3 regions were also remarkably abrogated, suggesting anti-apoptotic neuroprotection. Specifically, the phosphorylated (p)-eNOS/eNOS and p-Akt/Akt were also increased ( P < 0.01 and 0.001, respectively), indicating reciprocating activation of Akt-eNOS signaling upstream of NO. Conclusion: Spatiotemporally controlled US-triggered NO release by Au-PLGA/GSNO mitigates cerebral vasoconstriction, improves brain perfusion and confers anti-apoptotic neuroprotection post-CPR via reciprocating Akt-eNOS-NO signaling.

Effects of Tetramethylpyrazine on Neuronal Apoptosis in the Superficial Dorsal Horn in a Rat Model of Neuropathic Pain

2012 ◽  
Vol 40 (06) ◽  
pp. 1229-1239 ◽  
Author(s):  
Yu-Fang Leng ◽  
Xiang-Mei Gao ◽  
Shu-Xiu Wang ◽  
Yan-Hong Xing
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Sham Group ◽  
Male Rats ◽  
Spinal Dorsal ◽  
Post Operation ◽  
The Right

The Bennett and Xie (1988) model of chronic constriction injury (CCI) investigated the effects of tetramethylpyrazine (TMP) on neuropathic pain-associated behaviors and neuronal apoptosis in the spinal dorsal horn. Fifty-four male rats were randomly divided into sham (group S), CCI (group C) and TMP groups (group T). Each group was divided into subgroups (n = 6 in each group) according the time of sacrifice: 3 d, 7 d and 14 d. Rat sciatic nerves were unligated (group S), or the right sciatic nerve was loosely ligated (groups C and T) to produce CCI. Mechanical withdrawal thresholds (MWTs) and thermal withdrawal latencies (TWLs) were measured, and the rats were sacrificed at different time points post-operation. The L4-L6 sections of the spinal cord were removed. Apoptotic changes were evaluated using the TUNEL method. Immunohistochemistry assessed Bcl-2 and caspase-3 expression. TMP treatment increased MWT and TWL values and Bcl-2 expression, but it reduced neuronal apoptosis and caspase-3 expression in laminae I–II of the spinal dorsal horn. These results suggested that the inhibition of neuronal apoptosis via the modulation of Bcl-2 and caspase-3 proteins in the rat spinal dorsal horn contributed to TMP-induced analgesia.

scholarly journals Trichostatin A reduces nerve cell apoptosis in depressive rats by regulating CREB/BDNF signaling pathway

2021 ◽  
Vol 20 (9) ◽  
pp. 1875-1880
Author(s):  
Lianyu Jin ◽  
Ying Bao
Keyword(s):  
Cell Apoptosis ◽  
Caspase 3 ◽  
Sham Group ◽  
Trichostatin A ◽  
Mrna Levels ◽  
Model Group ◽  
Expression Levels ◽  
Immobility Time ◽  
Swimming Test ◽  
Bdnf Signaling

Purpose: To investigate the influence of trichostatin A on nerve cell apoptosis in depressive rats and to explore the probable molecular mechanism of action.Methods: A total of 36 Sprague-Dawley rats weighing 200 - 220 g were divided into sham group (n = 12), model group (n = 12) and trichostatin group (n = 12) by randomization. The protein expressions of phosphorylated cAMP responsive element-binding protein (p-CREB) and BDNF, as well as the mRNA expression levels of B-cell lymphoma-2 (Bcl-2) and caspase-3 in each group of rat hippocampus were determined by Western blotting and quantitative reverse transcription-polymerase chain reaction (qRTPCR), respectively. The apoptosis of nerve cells in the brain tissues of the rats was labeled using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.Results: Compared with those in the sham group, the degree of sucrose preference decreased markedly, while the immobility time after forced swimming test was extended, and the relative expression levels of p-CREB and BDNF proteins in the hippocampus declined (p < 0.05). The mRNA levels of Bcl-2 and caspase-3 and cell apoptosis rate were increased in the model group (p < 0.05). In comparison with the model group, the trichostatin group exhibited increased sucrose preference degree, shortened immobility time following a forced swimming test, and elevated relative expression levels p-CREB and BDNF proteins in the hippocampus (p < 0.05), but lowered mRNA levels of Bcl-2 and caspase-3 and cell apoptosis rate, displaying statistically significant differences (p < 0.05).Conclusion: Trichostatin A reduces cell apoptosis and ameliorates the depression-like behaviors of rats via the regulation of CREB/BDNF signaling pathway. These findings provide new insights into Trichostatin A for the management of depression.

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