Lidocaine activates autophagy of astrocytes and ameliorates chronic constriction injury-induced neuropathic pain

2020 ◽  
Author(s):  
Jiaqi Yuan ◽  
Yue Fei
Keyword(s):  
Cell Proliferation ◽  
Neuropathic Pain ◽  
Chronic Constriction Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Factor ◽  
Experimental Basis ◽  
Withdrawal Threshold ◽  
Withdrawal Latency ◽  
Tnf Α ◽  
Rat Astrocytes

Abstract Lidocaine is a commonly used drug to alleviate neuropathic pain (NP). This work aims to investigate the mechanism of lidocaine in alleviating NP. Chronic constriction injury (CCI) rats were established by surgery to induce NP. We observed the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) of rats. Immunofluorescence staining was performed to determine the LC3/glial fibrillary acidic protein (GFAP)-positive cells. Rat astrocytes were treated with lipopolysaccharide (LPS) to induce CCI, and then treated with lidocaine or 3-MA (autophagy inhibitor). CCK-8 was performed to detect cell proliferation. Western blot and enzyme-linked immunosorbent assay were performed to detect the level of protein and inflammatory factor. CCI rats exhibited a decrease of MWT and TWL, which was effectively abolished by lidocaine. Lidocaine enhanced the number of LC3/GFAP-positive cells in CCI rats. Moreover, lidocaine inhibited the expression of GFAP and p62, and enhanced LC3-II/LC3-I expression in the LPS-treated astrocytes. Lidocaine inhibited the level of TNF-α and IL-1β in the LPS-treated astrocytes. The influence conferred by lidocaine was effectively abolished by 3-MA. In conclusion, our work demonstrates that lidocaine activates autophagy of astrocytes and ameliorates CCI-induced NP. Thus, our study provides a further experimental basis for the mechanism of lidocaine to alleviate NP.

scholarly journals Pulsed Radiofrequency Reduced Neuropathic Pain Behavior in Rats Associated with Upregulation of GDNF Expression

2016 ◽  
Vol 19 (2;2) ◽  
pp. 49-58 ◽  
Author(s):  
Luo Fang
Keyword(s):  
Chronic Constriction Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pulsed Radiofrequency ◽  
Glia Cell ◽  
Group 14 ◽  
Time Points ◽  
Withdrawal Threshold ◽  
Withdrawal Latency ◽  
The Right ◽  
Ligation Site

Background: Pulsed radiofrequency (PRF) is a novel nondestructive interventional technique for the treatment of neuropathic pain (NP). However, this intervention is still lack of relevant regulation and the mechanism of action is insofar not clear. Historically, most studies have reported that PRF can relieve reduce hyperalgesia in multiple NP animal models by acting on the dorsal root ganglion. However, a few recent studies have shown that PRF can effectively treat hyperalgesia in pain models by a direct application on injured peripheral nerves. Objectives: To observe changes in pain behavior and the pathology of the sciatic nerve (SN) after applying PRF at the ligation site in a chronic constriction injury (CCI) rat model and to investigate the effect of PRF on the expression of glia cell line-derived neurotrophic factor (GDNF) in nervous tissue. Study Design: A randomized, experimental trial. Setting: Experimental Animal Center, Beijing Tiantan Hospital, Capital Medical University. Methods: Thirty-six adult Sprague-Dawley rats were randomly divided into 3 groups: Sham-Sham (SS), CCI-Sham (CS), and CCI-PRF (CP). The right SNs of the rats in the CS and CP groups were ligated to create a CCI model. For the SS group, the right SN was separated without ligation. On the 14th fourteenth day after surgery, PRF treatment was applied at the ligation site of the SN for the rats in the CP group using a 45 V output voltage at 42°C for 3 minutes. The electrode was placed in rats in the SS and CS groups without electricity applied. The hindpaw withdrawal threshold (HWT) and thermal withdrawal latency (TWL) were measured at various time points before and after the treatments in each group. Optical microscopic scores and electron microscopic observation were given to the right SN ligation sites of the rats in each group 14 days after the treatment . Meanwhile, the GDNF expression levels in the ligation site of the SN and in the L4-L6 spinal cord segments were determined for each group by enzyme-linked immunosorbent assay (ELISA). Results: Fourteen days after PRF treatment, the HWT and TWL values in the CP group were significantly increased compared to those of the CS group (P < 0.01). Under the optical microscope, the axonal number, axonal diameter, and myelin sheath thickness in the CP group were significantly increased compared to those of the CS group 14 days after PRF treatment (P < 0.01). Under the electron microscope, the degeneration at the SN ligation site was significantly improved in the CP group compared to the CS group. The GDNF expression levels at the ligation site of the SN and the L4-L6 spinal segments in the CP and CS groups were increased compared to those of the SS group (P < 0.01). In addition, the GDNF expression in the CP group was significantly higher than that in the CS group (P < 0.01). Limitations: GDNF expression was only measured at day 14 after the treatment rather than at various time points during the experiment. Conclusions: The findings suggest that the application of PRF at the impaired SN relieved reduced the CCI-induced NP by through regulating the upregulation of the GDNF expression in the nervous tissues. Key words: Pulsed radiofrequency, chronic constriction injury, sciatic nerve, spinal cord, hind paw withdrawal threshold, thermal withdrawal latency, optical microscopic, electron microscope, glia cell line-derived neurotrophic factor, enzyme-linked immunosorbent assay

scholarly journals Dezocine attenuates neuropathic pain by inhibiting ERK1/2 signaling in rats

2019 ◽  
Author(s):  
Chan Shen ◽  
Shi Sheng ◽  
Ling Yu ◽  
Naixing Xin
Keyword(s):  
Neuropathic Pain ◽  
Quantitative Polymerase Chain Reaction ◽  
Mammalian Target Of Rapamycin ◽  
Life Quality ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Expression Levels ◽  
Withdrawal Threshold ◽  
Tnf Α ◽  
Cox 2

Abstract Background Neuropathic pain severely impacts patients’ life quality. Dezocine can be used for the treatment of pain. The present study intended to explore the effects of dezocine in chronic constriction injury (CCI) induced neuropathic pain as well as the possible responsible molecules in rats. Methods There were 3 subgroups, ie, control group, CCI group and dezocine+CCI group. The values of paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) in rats were determined by a dynamic plantar esthesiometer. The ipsilateral lumbar spinal cords in rats were extracted for the detection of protein levels of phosphorylated-mammalian target of rapamycin (p-mTOR) and p-extracellular signal-regulated kinase 1/2 (p-ERK1/2) by western blot analysis; and the mRNA and protein expression levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, and cyclooxygenase-2 (COX-2) by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Results In comparison with control group, there were lower values of PWT and PWL in CCI group, which were partially reversed by dezocine. In addition, compared to control group, the expression levels of p-mTOR, p-ERK1/2, IL-6, TNF-α and COX-2 were upregulated by CCI, which were attenuated by dezocine. Conclusions In conclusion, the analgesic effect of dezocine on CCI induced neuropathic pain might be correlated with inhibiting of the p-mTOR and p-ERK1/2 signaling pathway.

scholarly journals Vitexin alleviates neuropathic pain in a mouse chronic constriction injury model by inactivation of NF-κB

2020 ◽  
Vol 19 (5) ◽  
pp. 989-994
Author(s):  
Wentong Xu ◽  
Xueli Zhu ◽  
Gonghao Zhan ◽  
Liangyu Sheng ◽  
Yanwei Chen
Keyword(s):  
Neuropathic Pain ◽  
Inflammatory Cytokines ◽  
Chronic Constriction Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Mechanical Hypersensitivity ◽  
Withdrawal Threshold ◽  
Before And After ◽  
Cci Model ◽  
Pro Inflammatory Cytokines

Purpose: To investigate the therapeutic effect of vitexin on neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI).Methods: The CCI model was established by four chronic ligatures in the sciatic nerve. Vitexin was intraperitoneally administered (10 mg/kg, once daily) for 21 days. Mechanical withdrawal threshold (MWT) and paw withdrawal latency (PWL) were determined before and after the establishment of CCI model. The spinal cords were collected to measure mRNA levels by reverse-transcriptase polymerase chain reaction (RT-PCR) enzyme-linked immunosorbent assay (ELISA). Western blot was used to examine protein expression levels.Results: Vitexin reversed the CCI-induced reduction in MWT and PWL values, indicating that it lowered mechanical hypersensitivity response and hyperalgesia caused thermal stimulation (p < 0.05). The elevated levels of IL-6, IL-1β, and TNFα observed in CCI-treated mice were also inhibited by vitexin, suggesting that it suppressed pro-inflammatory cytokines. Moreover, vitexin attenuated CCI-induced activation of NF-κB signaling in CCI-treated mice (p < 0.05).Conclusion: Vitexin alleviates NP by inhibiting pro-inflammatory cytokines and NF-κB signaling in CCItreated mice. Thus, it is a potential target for NP treatment. Keywords: Vitexin, Neuropathic pain, Chronic constriction injury, Mechanical hypersensitivity, Hyperalgesia, NF-κB

scholarly journals Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis

2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Zhen Li ◽  
Aiyuan Li ◽  
Liping Yan ◽  
Tian Yang ◽  
Wei Xu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Noncoding Rna ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Withdrawal Threshold ◽  
Downstream Target ◽  
Tnf Α ◽  
Close Relationship

Abstract Background Neuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models. Methods We first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin‐6 (IL-6), tumor necrosis factor‐α (TNF-α) and IL-1β. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays. Results Our findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL‐6, IL‐1β and TNF‐α in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats. Conclusion DLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.

scholarly journals POS1290 CYTOKINE BIOMARKERS IN COMMON LOW BACK PAIN

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 926.3-926
Author(s):  
R. Dhahri ◽  
A. Dghaies ◽  
M. Slouma ◽  
L. Metoui ◽  
I. Gharsallah ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Low Back Pain ◽  
Back Pain ◽  
Inflammatory Cytokines ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Controls ◽  
Low Back ◽  
Tnf Α ◽  
Functional Scores ◽  
The Mean

Background:Common low back pain (LBP) is a common health problem affecting 50 to 80% of working age adults. It is one of the common and costly health problems in Tunisia. Actually, the role of the immune response and inflammatory cytokines in the pathogenesis of chronic pain has been of growing interest.Objectives:The aim of this study was to assess whether pro and anti-inflammatory cytokines could be detected in serum in patients with LBP compared with healthy subjects and whether they could be related to pain severity and to clinical findings.Methods:It was a an analytical cross-sectional study including 50 patients with at least three months of LBP, in the department of rheumatology, orthopedics and immunology at the Military Hospital of Tunis between January 1st and March 31, 2020. All patients had a standardized clinical assessment.Levels of serum cytokines IL-6, IL-8, IL-1β and TNF- α, were measured using the chimiluminescence technique. Serum concentration of IL-10 was assayed by the enzyme-linked immunosorbent assay technique (ELISA). The normal levels of cytokines were determined in 50 healthy controls.Results:The mean age of the patients was 41.9 ± 8.4 years and the sex ratio was 4.5. LBP duration was 66.4 months. The mean lumbar visual analog scale (VAS) was 4.5 ± 1.9, and the root VAS was 2.6 ± 2.5. Neuropathic pain was found in 26% of patients. The average BMI was 27 ± 3.7 kg/m2. Only serum level of IL-8 was significantly higher in subjects with LBP compared to healthy controls (p <10-3). IL-1β was indetectable in both patients and controls. Positive correlations were found between IL-8 levels and anxiety/functional scores (r = 0.3; p = 0.02/ r = 0.3; p = 0.04). IL-6 was positively correlated with BMI, and negatively correlated with the Schober test. No correlations were found between serum levels of IL-6, IL-8, IL-10, TNF-α and pain intensity (VAS), neuropathic pain (DN4), fibromyalgia (FIRST), depression (HAD) and various radiological data.Conclusion:Interleukin-8 is a biomarker of common low back pain and correlate with anxiety and functional disability. These results suggest that IL-8 may be a therapeutic target to reduce chronic back pain and reduce the social and profession impact.Disclosure of Interests:None declared

scholarly journals MiR-1906 attenuates neuropathic pain in rats by regulating the TLR4/mTOR/ Akt signaling pathway

2019 ◽  
Vol 10 (1) ◽  
pp. 175-179 ◽  
Author(s):  
Xianhai Fang ◽  
Huacheng Zhou ◽  
Shaopeng Huang ◽  
Jinfeng Liu
Keyword(s):  
Neuropathic Pain ◽  
Western Blotting ◽  
Rat Model ◽  
Latency Period ◽  
Enzyme Linked Immunosorbent Assay ◽  
Withdrawal Latency ◽  
Proinflammatory Mediators ◽  
Neuropathic Pain Model ◽  
Pathway Regulation

Abstract Background This study determined the role of miR-1906 in neuropathic pain and proliferation in neuronal cells using a chronic constriction injury (CCI)-induced neuropathic pain (NP) rat model. Methodology NP was induced by CCI. Animals were divided into a sham group, an NP group, and a miR-1906 mimic group, which received 500 nmol/kg of a miR-1906 mimic intrathecally for 10 consecutive days following surgery. The effect of miR-1906 agomir was determined by estimating the thermal and mechanical withdrawal latency; an enzyme-linked immunosorbent assay (ELISA) was used to determine the concentration of proinflammatory mediators. Western blotting and reverse-transcription polymerase chain reaction (RT-PCR) were used to determine protein expression in the spinal tissues of the CCI-induced neuropathic pain rat model. Results Administration of miR-1906 agomir increased the mechanical and thermal withdrawal latency period and the levels of inflammatory mediators compared with the NP group. Western blotting showed that treatment with miR-1906 agomir attenuated the levels of Akt, mTOR, TLR-4, and PI3K proteins in the spinal tissues of the CCI-induced neuropathic pain model. TLR-4 and NF-κB gene expression was lower in the miR-1906 agomir group than in the NP group. Conclusion miR-1906 gene stimulation reduced neuropathic pain by enhancing Akt/nTOR/PI3K and TLR-4/NF-κB pathway regulation.

LncRNA PCAT19 Regulates Neuropathic Pain via Regulation of miR-182-5p/JMJD1A in a Rat Model of Chronic Constriction Injury

2021 ◽  
pp. 1-9
Author(s):  
Miao Huo ◽  
Xingxing Zheng ◽  
Ning Bai ◽  
Ruifen Xu ◽  
Guang Yang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Rat Model ◽  
Noncoding Rna ◽  
Thermal Hyperalgesia ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Inflammatory Factor ◽  
Reporter Assay ◽  
Withdrawal Threshold ◽  
Dual Luciferase Reporter Assay

<b><i>Introduction:</i></b> Neuropathic pain (NP) is one of the most severe chronic pain types. In recent years, more and more studies have shown that long noncoding RNA (LncRNA) plays a key role in a variety of human diseases, including NP. However, the role of LncRNA prostate cancer-associated transcript 19 (PCAT19) in NP and its specific mechanism remain unclear. <b><i>Methods:</i></b> A chronic constrictive injury (CCI) rat model was established. Rat paw withdrawal threshold and paw withdrawal latency were used to evaluate the neuronal pain behavior of rats in this model. mRNA expression of PCAT19, neuroinflammatory factor, microRNA (miR)-182-5p, and Jumonji domain containing 1A (JMJD1A) were detected by quantitative real-time PCR. ELISA analysis was used to detect inflammatory factor protein expression. Dual-luciferase reporter assay was used to evaluate the targeting relationship between genes. <b><i>Results:</i></b> PCAT19 was continuously upregulated in CCI rats. miR-182-5p was the target of PCAT19, and miR-182-5p was increased after PCAT19 knockdown. NP behaviors such as mechanical ectopic pain and thermal hyperalgesia as well as neuroinflammation can be reduced by knocking down PCAT19. However, the injection of miR-182-5p antagomir significantly reversed the level of the NP behaviors and neuroinflammation caused by PCAT19 knockdown. Besides, dual-luciferase reporter assay showed that JMJD1A was the target gene of miR-182-5p. The level of JMJD1A in CCI rats increased with time. After PCAT19 knockdown, JMJD1A was significantly decreased, but inhibition of miR-182-5p can reverse its levels. <b><i>Conclusion:</i></b> This study shows that PCAT19 plays a role in NP by targeting the miR-182-5p/JMJD1A axis, and PCAT19 can be used as a new therapeutic target for NP.

scholarly journals Effects of Hyperbaric Oxygen on Pain-Related Behaviours and Nitric Oxide Synthase Expression in a Rat Model of Neuropathic Pain

2013 ◽  
Vol 18 (3) ◽  
pp. 137-141 ◽  
Author(s):  
Guang Han ◽  
Lu Li ◽  
Ling-xin Meng
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Neuropathic Pain ◽  
Nitric Oxide Synthase ◽  
Hyperbaric Oxygen ◽  
Rat Model ◽  
Withdrawal Threshold ◽  
Withdrawal Latency ◽  
Oxide Synthase ◽  
Inducible Nos

BACKGROUND: Neuropathic pain is complex, and a satisfactory therapeutic method of treatment has yet to be developed; therefore, finding a new and effective therapeutic method is an important issue in the field of neuropathic pain.OBJECTIVE: To determine the effects of hyperbaric oxygen (HBO) on pain-related behaviours and nitric oxide synthase (NOS) expression in a rat model of neuropathic pain.METHODS: Forty male Sprague Dawley rats were randomly divided into five groups (eight rats per group) including control, sham operation, sciatic nerve with chronic constriction injury (CCI), HBO pretreatment (pre-HBO) and HBO post-treatment (post-HBO) groups. Pain-related behaviours and NOS expression in the spinal cord were compared among the five groups.RESULTS: Compared with the CCI group, the mechanical withdrawal threshold was significantly increased and thermal withdrawal latency was significantly extended in the pre-HBO and post-HBO groups (all P<0.05). After CCI, expression of spinal neuronal NOS and inducible NOS were increased. Expression of spinal neuronal NOS and inducible NOS were significantly decreased in the pre-HBO and post-HBO groups compared with the CCI group (all P<0.05). Spinal eNOS expression changed very little.DISCUSSION: HBO has been used as an effective and noninvasive method for the treatment of spinal cord injuries and high-altitude sickness, and in immunosuppression and stem-cell research; however, it has yet to be applied to the treatment of neuropathic pain. The present study indicated that HBO effectively increased mechanical withdrawal threshold and thermal withdrawal latency, demonstrating that HBO has therapeutic effects on neuropathic pain.CONCLUSION: HBO inhibits pain in rats with CCI through the regulation of spinal NOS expression.

scholarly journals Dynamic effects of TNF-α on synaptic transmission in mice over time following sciatic nerve chronic constriction injury

2013 ◽  
Vol 110 (7) ◽  
pp. 1663-1671 ◽  
Author(s):  
Hongmei Zhang ◽  
Haijun Zhang ◽  
Patrick M. Dougherty
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Sciatic Nerve ◽  
Synaptic Transmission ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Chronic Constriction Injury ◽  
Synaptic Signaling ◽  
Tnf Α ◽  
Over Time

Nerve injury-induced central sensitization can manifest as an increase in excitatory synaptic transmission and/or as a decrease in inhibitory synaptic transmission in spinal dorsal horn neurons. Cytokines such as tumor necrosis factor-α (TNF-α) are induced in the spinal cord under various injury conditions and contribute to neuropathic pain. In this study we examined the effect of TNF-α in modulating excitatory and inhibitory synaptic input to spinal substantia gelatinosa (SG) neurons over time in mice following chronic constriction injury (CCI) of the sciatic nerve. Whole cell patch-clamp studies from SG neurons showed that TNF-α enhanced overall excitability of the spinal cord early in time following nerve injury 3 days after CCI compared with that in sham control mice. In contrast, the effects of TNF were blunted 14 days after CCI in nerve-injured mice compared with sham surgery mice. Immunohistochemical staining showed that the expression of TNF-α receptor 1 (TNFR1) was increased at 3 days but decreased at 14 days following CCI in the ipsilateral vs. the contralateral spinal cord dorsal horn. These results suggest that TNF-α acting at TNFR1 is important in the development of neuropathic pain by facilitating excitatory synaptic signaling in the acute phases after nerve injury but has a reduced effect on spinal neuron signaling in the later phases of nerve injury-induced pain. Failure of the facilatory effects of TNF-α on excitatory synaptic signaling in the dorsal horn to resolve following nerve injury may be an important component in the transition between acute and chronic pain conditions.

Protective effects of diosmetin extracted from Galium verum L. on the thymus of U14-bearing mice

2011 ◽  
Vol 89 (9) ◽  
pp. 665-673 ◽  
Author(s):  
Rui Zhao ◽  
Zhibao Chen ◽  
Guiyan Jia ◽  
Jian Li ◽  
Yaping Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Proliferation Assay ◽  
Cell Proliferation Assay ◽  
Tnf Α ◽  
Thymus Tissue ◽  
Tgf Β1

Diosmetin (DGVL) extracted from the traditional Chinese herb Galium verum L. has been found to have anticancer activity. In this study, the effects of DGVL on the thymus of U14-bearing mice were investigated. Using flow cytometry, peripheral blood lymphocytes were characterized based on the expression of surface markers for T helper cells (CD4+) and T suppressor cells (CD8+). Serum levels of tumor necrosis factor α (TNF-α), interleukin-2 (IL-2), IL-10, and transforming growth factor β1 (TGF-β1) and a cell proliferation assay were determined with an enzyme-linked immunosorbent assay. The expression of Fas and Fas ligand (FasL) on the thymus was determined by Western blotting. Our results showed that DGVL inhibited tumor growth and significantly increased the thymus weight compared with the control. Also, DGVL elevated serum levels of IL-2 and significantly reduced levels of TNF-α, TGF-β1, and IL-10 in a dose-dependent manner. Histological study and terminal dUTP nick end labeling staining results showed that DGVL protected thymus tissue against the onslaught of tumor growth by inhibiting thymus lymphocyte apoptosis. The cell proliferation assay revealed that DGVL might promote more thymus lymphocytes towards proliferation. Furthermore, the ratio of CD4+/CD8+ T lymphocytes was significantly increased from 0.69 to 2.29 by treatment with DGVL. Immunoblotting analyses revealed that the expression of Fas and FasL on the thymus was lower in mice in the DGVL treatment group than in the control mice. In conclusion, DGVL can inhibit tumor growth and protect tumor-induced apoptosis of the thymus, and the mechanism is closely associated with reduced cell death in the thymus and a Fas–FasL-dependent pathway.

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