Behavioural, metabolic, and endothelial effects of the TNF-α suppressor thalidomide on rats subjected to chronic mild stress and fed an atherogenic diet

2014 ◽  
Vol 92 (5) ◽  
pp. 375-385 ◽  
Author(s):  
Basma Ismail ◽  
Sawsan Aboul-Fotouh ◽  
Amal A. Mansour ◽  
Hanan H. Shehata ◽  
Manal I. Salman ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Chronic Mild Stress ◽  
Atherogenic Diet ◽  
Control Group ◽  
Mild Stress ◽  
Rt Pcr ◽  
Treatment Groups ◽  
Tnf Α ◽  
Induced Changes ◽  
Endothelial Dysfunctions

There is accumulating evidence suggesting that depression is a risk factor for cardiovascular diseases. This study aimed to examine the hypothesis that the proinflammatory cytokine TNF-α would partially explain the link between depression and atherosclerotic endothelial changes. Rats were distributed among 6 groups: (i) control group; (ii) group subjected to chronic mild stress (CMS); (iii) group fed a cholesterol–cholic acid–thiouracil (CCT diet); and (iv) CMS group fed the CCT diet and treated with the vehicle for 8 weeks. The last 2 groups were subjected to CMS–CCT and received thalidomide (THAL) or imipramine (IMIP). Rats were assessed behaviorally (sucrose preference, open field, and forced-swimming tests). TNF-α protein was assessed from the serum, aorta, and liver. Aortic TNF-α gene expression (assessed using RT–PCR), serum lipid profile, and insulin levels were measured. Endothelial function was assessed in isolated aortic rings. The THAL and IMIP groups showed ameliorated CMS–CCT-related behavioral changes. CMS–CCT-induced metabolic and endothelial dysfunctions were improved in the THAL group but were worsened in the IMIP group. RT–PCR showed a significant reduction of aortic TNF-α mRNA expression in the THAL and IMIP treatment groups. These data paralleled the findings for aortic immunohistochemistry. The THAL group, but not the IMIP group, showed improved CMS–CCT-induced changes in the vascular reactivity of the aortic rings. Thus, TNF-α provides a target link between depression, metabolic syndrome, and endothelial dysfunction. This could open a new therapeutic approach to address the comorbidities of depression.

scholarly journals The Role of Bamboo Shoot Gigantochloa apus Extract in Decreasing MDA and Increasing IL-10 at The Atherosclerosis

2019 ◽  
Vol 3 (1) ◽  
pp. 23-27
Author(s):  
Edy Soesanto ◽  
Edi Dharmana ◽  
Soeharyo Hadisaputro ◽  
Siti Fatimah Muis
Keyword(s):  
Atherogenic Diet ◽  
Control Group ◽  
Antioxidant Compounds ◽  
Bamboo Shoot ◽  
Control Group Design ◽  
Treatment Groups ◽  
New Zealand White Rabbits ◽  
Post Test ◽  
Free Radical Formation

Introduction: Bamboo shoot Gigantochloa apus extract has antioxidant compounds that act as lipid peroxidation inhibitors and reduce free radical formation so that it can be used as an anti-inflammatory and anti-oxidative stress in the atherosclerosis. Aim: Knowing the effect of bamboo shoot Gigantochloa apus extract in reducing MDA levels and IL-10 increasing levels in rabbits given atherogenic diet. Methods: This experiment used randomized pre-test and post-test with control group design, in 24 New Zealand White rabbits divided into 4 groups randomly. MDA and IL-10 levels were examined by the ELISA method. Results and conclusion: Bamboo shoot Gigantochloa apus extract can reduce MDA levels and increase IL-10 levels significantly in accordance with increasing doses. The increase of MDA levels in the control group with all treatment groups was different (p = 0.0001), and between the treatment groups and other treatment groups there were also differences (p

Electroacupuncture Prevents the Depression-Like Behavior by Inhibiting the NF-κB/NLRP3 Inflammatory Pathway in Hippocampus of Mice Subjected to Chronic Mild Stress

2022 ◽  
pp. 1-9
Author(s):  
Qi Wang ◽  
Hongsheng Bi ◽  
Hongfei Huang ◽  
Yitong Wang ◽  
Lili Gong ◽  
...  
Keyword(s):  
Chronic Mild Stress ◽  
Preference Test ◽  
Underlying Mechanism ◽  
Sucrose Preference ◽  
Receptor Protein ◽  
Mild Stress ◽  
Inflammatory Pathway ◽  
Protein Levels ◽  
Tnf Α ◽  
Immobility Time

<b><i>Background:</i></b> The precise physiological mechanisms of acupuncture in the treatment of depression are still unknown. This study aimed to observe the effects of electroacupuncture (EA) on depression-like behavior of mouse in chronic mild stress (CMS) model and explore the underlying mechanism. <b><i>Methods:</i></b> The depression model was established by using CMS method for 6 weeks. After the third week of the CMS paradigm, EA treatment was performed daily for 15 min over a period of 3 weeks. The antidepressant-like effects of EA were evaluated using the sucrose preference test and the forced swimming test (FST). The protein levels of the nuclear factor-kappa B (NF-κB), p-NF-κB, inhibitor of NF-κB, p-IκBα, NOD-like receptor protein 3, interleukin (IL)-6, IL-1β, IL-18, and tumor necrosis factor-α (TNF-α) in hippocampus of mice were detected. <b><i>Results:</i></b> Sucrose preference was decreased after 6 weeks of CMS and the effects of CMS was reversed by EA. CMS increased immobility time and decreased latency to the first immobility in the FST test, but these effects were reversed by EA. CMS-induced nuclear entry of NF-κB (nuclear/cytoplasmic ratio of NF-κB) with an increase in protein levels of p-NF-κB and p-IκBα in the hippocampus. The CMS also increased NLRP3 levels in the hippocampus. However, these effects were reversed by EA. In addition, the levels of IL-6, IL-1β, IL-18, and TNF-α in the hippocampus were increased by CMS, and these effects of stress were reversed by EA. <b><i>Conclusion:</i></b> EA prevented CMS-induced depressive-like behaviors by inhibiting NF-κB/NLRP3 inflammatory pathway.

scholarly journals Anti-Inflammatory Effect of Musa acuminata Stem

2020 ◽  
Vol 14 (02) ◽  
pp. 294-298
Author(s):  
Maharani Laillyza Apriasari ◽  
Selviana Rizky Pramitha ◽  
Dewi Puspitasari ◽  
Diah Savitri Ernawati
Keyword(s):  
Treatment Group ◽  
Musa Acuminata ◽  
Control Group ◽  
Control Group Design ◽  
Treatment Groups ◽  
Tnf Α ◽  
Significant Difference ◽  
Anti Inflammatory ◽  
Mucosal Wound ◽  
Inflammatory Effect

Abstract Objective This study was designed to assess the anti-inflammatory effect of Musa acuminata through the expression of tumor necrosis factor-α (TNF-α) and nuclear factor kappa β (NF-κB) after 3 days of application of Musa acuminata stem extract (MASE) gel on oral mucosal wound. Materials and Methods An experimental study with post-test only control group design was conducted. Twenty male Rattus norvegicus (Wistar) were injured on their left buccal mucosa and treated three times a day with MASE gel of varying concentrations: 0% (as control), MASE 25%, MASE 37.5%, and MASE 50%. On day 3, a biopsy was performed on each mucosal wound for later immunohistochemical analysis for the expressions of TNF-α and NF-κB. Results The highest expression of TNF-α was observed in the control group (13.20 ± 1.79), while the lowest was in the treatment group using 50% MASE (6.40 ± 1.14). Meanwhile the comparison between treatment groups did not highlight any significant difference (p > 0.05). The highest expression of NF-κB was observed in the control group (13.20 ± 1.30), whereas the lowest was in the treatment group using MASE 50% (6.40 ± 1.14). NF-κB was significantly lower in the treatment group using MASE 50% when compared with other treatment groups (p < 0.05). Conclusion Application of MASE on mucosal wound reduces the expression of TNF-α and NF-κB at all concentrations. The anti-inflammatory effect of MASE 50% was the strongest one.

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

scholarly journals Heat stress combined with lipopolysaccharide alter the activity and superficial molecules of peripheral monocytes

2019 ◽  
Vol 33 ◽  
pp. 205873841982889
Author(s):  
Jiajing Luo ◽  
Yi Chen ◽  
Chengjia Ding ◽  
Jialing Qiu ◽  
Yulan Chen ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Heat Stress ◽  
Western Blot ◽  
Inflammatory Mediators ◽  
Peripheral Blood ◽  
Heat Stroke ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Rt Pcr ◽  
Tnf Α

The purpose of this study was to focus on the underlying relationship between the hyperactivity for the peripheral monocytes and heat stroke by investigating the inflammatory oxidative activity of and the expression of superficial molecules. Peripheral blood samples were collected from 10 healthy adult volunteers. Human blood monocytes were isolated by density gradient centrifugation and sequent adherent culture. The objectives were divided into four groups: 43°C heat stress combined with lipopolysaccharide (LPS) group, 43°C heat stress group, LPS group, and control group. There were 10 cases in each group. An enzyme-linked immunosorbent assay (ELISA) test was used to measure the concentrations of supernatant inflammatory mediators (tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10)). After loaded by 2,7-Dichlorodi-hydrofluorescein-diacetate (DCFHDA) fluorescent probe, intracellular reactive oxygen species (ROS) levels were determined by a flow cytometry. After fluorescent microspheres incubation, the phagocytosis of monocytes was observed under a fluorescent microscope. Respectively, the flow cytometry and Western blot were used to evaluate the level of triggering receptor expressed on myeloid cells-1 (TREM-1) and Toll-like receptor-4 (TLR-4) on the monocytes. Furthermore, the mRNA expression of TREM-1 and TLR-4 was detected by real-time polymerase chain reaction (RT-PCR). The heat stress combined with LPS stimulation promoted the peripheral monocytes to produce inflammatory mediators (TNF-α, IL-1β, and IL-10) and release ROS. Otherwise, such complex strike significantly suppressed the phagocytic activity of monocytes in peripheral blood. Moreover, the expression of TREM-1, TLR-4 and CD86 was measured by the flow cytometry on peripheral monocytes which were respectively promoted by the union of heat stress and LPS. The results of Western blot and RT-PCR demonstrated the similar kinetics on these superficial molecules (TREM-1, TLR-4, and CD86) stimulated by the combination of heat stress and LPS. The underlying mechanism of the dysfunction for the peripheral monocytes may be related to the abnormal expression of superficial molecules TREM-1, TLR-4, and CD86 on the monocytes induced by heat stress and LPS.

Study on Mechanism of Human Marrow Mesenchymal Stem Cell in Treating Patients with Aplastic Anemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4099-4099
Author(s):  
Zhenhua Qiao ◽  
Xiujuan Zhao
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
T Cells ◽  
Aplastic Anemia ◽  
Hematopoietic Cell ◽  
Control Group ◽  
Rt Pcr ◽  
Tnf Α ◽  
Ifn Γ ◽  
Tgf Β1

Abstract Objective: To explore mechanism of human marrow mesenchymal stem cells (MSCs) in treating patients with aplastic anemia(AA). Methods: MSCs in patients with aplastic anemia(AA) and the control group were separated with Percoll(1.073g/m L) and cultured in low glucose DMEM. Then, observed their morphologies,checked their molecule surface antigen by flow cytometry and examined the process of adipogenic differention. The mononuclear cells (MNC)of marrow in patients with AA were enriched based 1.077g/L density centrifuge and cultured in the 1640 medium. (1)MSC in control group and MNC in AA group were co-cultured with or without cytokines. The function of supporting hematopoiesis for MSC was to be observed in single confluence layer after plating by counting the total cells and the clones in every well every week. Then analyzed the dynamics of proliferation. T cells were harvested by using nylon column. MSC in control group and T cells in AA group were co-cultured. The proliferation of T cell was measured by MTT method. The CD25,CD69,CD4,CD8,Annexin-V expression rates of CD3+T cells were analyzed by flow cytometry .The gene and protein of IL-2, IL-4,IL-10,TNF-α,IFN-γ,TGF-β1 were examined by RT-PCR and ELISA respectively. MSC treated to the model of AA, by the examination of peripheral hemogram, bone marrow biopsy, pathological section of spleen. Results: There was no significant difference between control group MSC and AA-MSC in morphologies but adipogenic differentiation in AA patients is earlier than controls. The clones of CFU-GM in group(MSC)(78.46±3.58)/2×105 cells, after 14 days cultured was significantly higher than(9.21±4.32)/2×105 cells in group(CK + DMEM medium), while lower than (99.32±4.34)/2×105 cells in group(MSC+CK). (1)the Treg cells (TCD4+CD25+) in AA group (2.01±1.21)/ 2×105 was significantly lower than (4.43±1.67)/2×105 cells in control group, while(5.43±2.31) / 2×105 in group (MSC+AAT) was no more than (4.43±1.67)/2×105 cells in control group. (2) MSCs significantly inhibited T cell proliferation (P< 0. O5)by MTT. (3) RT-PCR and ELISA analysis showed that MSCs induced the expression of IL-4, IL-10, TGF-β1 and decreased significantly the expression of IL-2, TNF-α, IFN -γ in T cells of AA. the model of AA treated by MSCs showed improvements in 3 blood components greatly(p<0.05), Bone marrow proliferated and restored to the normal level, hematopoietic cell increased obviously (hematopoietic cell capacity was more than 40%), and atrophied spleen restore to normality. Conclusions: morphologies of AA’MSC had no evident different with the control but was more easy adipogenic differention. aplastic anemia belongs to autoimmune diseases in which T cells effect organ-specific destruction. The fundamental mechanism of MSC in treating AA should be potential to promote hematopoietic cell proliferation by adjusting immunity.

Protein-free phospholipid emulsion treatment improved cardiopulmonary function and survival in porcine sepsis

2003 ◽  
Vol 284 (2) ◽  
pp. R550-R557 ◽  
Author(s):  
Roy D. Goldfarb ◽  
Thomas S. Parker ◽  
Daniel M. Levine ◽  
Dana Glock ◽  
Imran Akhter ◽  
...  
Keyword(s):  
Density Lipoprotein ◽  
Fibrin Clot ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Serum Lipoproteins ◽  
Treatment Groups ◽  
Tnf Α ◽  
Dose Dependent

Lipoprotein phospholipid (PL) plays a major role in neutralization of endotoxin. This study tested the hypothesis that prophylactic administration of a PL-enriched emulsion (PRE), which augments PL content of serum lipoproteins and neutralizes endotoxin in vitro, would preserve cardiovascular function and improve survival in porcine septic peritonitis. A control group was compared with low-, mid-, and high-dose treatment groups that received PRE by primed continuous infusion for 48 h. A fibrin clot containing live Escherichia coli 0111.B4 was implanted intraperitoneally 30 min after the priming dose. Survival increased in a dose-dependent manner and was correlated with serum PL. Infused PL was associated with high-density lipoprotein in the low-dose group and all serum lipoproteins at higher doses. Treatment significantly lowered serum endotoxin and tumor necrosis factor (TNF)-α, preserved cardiac output and ejection fraction, and attenuated increases in systemic and pulmonary vascular resistances. This study demonstrated that augmentation of lipoprotein PL via administration of PRE improved survival and offered a novel therapeutic approach to sepsis.

scholarly journals Dachengqi Decoction Attenuates Intestinal Vascular Endothelial Injury in Severe Acute Pancreatitis in Vitro and in Vivo

2017 ◽  
Vol 44 (6) ◽  
pp. 2395-2406 ◽  
Author(s):  
Li-yun Pan ◽  
Ya-feng Chen ◽  
Hong-chang Li ◽  
Li-ming Bi ◽  
Wen-jie Sun ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Serum Amylase ◽  
Endothelial Damage ◽  
Intestinal Injury ◽  
Control Group ◽  
Rt Pcr ◽  
Intestinal Tissue ◽  
Tnf Α

Background/Aims: Dachengqi decoction (DCQD) is a well-known traditional Chinese herbal drug with strong anti-inflammatory effects. Angiopoietin-1 (Ang-1) plays a vital role in maintaining the stability and integrity of the vascular wall and prevents vascular leakage due to inflammatory mediators. Our previous work found that DCQD protects against pancreatic injury in rats with severe acute pancreatitis (SAP). This study aims to investigate the effects of DCQD on intestinal endothelial damage in both damaged human umbilical vein endothelial cells (HUVECs) and SAP rats. Methods: HUVECs were randomly divided into four groups: control group, TNF-α group, TNF-α plus Ang-1 group (Ang-1 group), and TNF-α plus DCQD group (DCQD group). Cells were incubated for 6 h, 12 h, and 24 h, before collection. The treatment concentration of DCQD was decided based on a Cell Counting Kit-8 (CCK-8) assay. The monolayer permeability of the HUVECs was assessed by measuring the transendothelial electrical resistance (TEER). Apoptosis was analyzed by flow cytometry. mRNA and protein expression of aquaporin 1 (AQP-1), matrix metalloproteinase 9 (MMP9), and junctional adhesion molecule-C (JAM-C) was evaluated by RT-PCR, immunocytofluorescence, and western blot. Forty male Sprague-Dawley rats were randomized into a control group, SAP group, SAP plus Ang-1 group (Ang-1 group), and SAP plus DCQD group (DCQD group). SAP was induced by intraperitoneal injection of cerulein and lipopolysaccharide (LPS), while the control group received 0.9% saline solution. Evans blue was injected through the penile vein and the rats were then sacrificed 12 h after modeling. Levels of serum amylase, TNF-α, IL-1β, IL-2, and IL-6 were determined by using ELISA. Intestinal tissue was analysed by histology, and capillary permeability in the tissues was evaluated by Evans blue extravasation assay. Protein and mRNA expression of AQP-1, MMP9, and JAM-C were assessed by immunohistofluorescence, western blot, and RT-PCR. Results: DCQD reduced the permeability of HUVEC induced by TNF-α in vitro. Furthermore, DCQD altered the mRNA and protein levels of JAM-C, MMP9, and AQP-1 in HUVECs after TNF-α induction. SAP intestinal injury induced by cerulein combined with lipopolysaccharides was concomitant with increased expression of JAM-C and MMP9, and reduced expression of AQP-1 in intestinal tissue. Pretreatment with DCQD attenuated SAP intestinal injury and lowered the levels of serum amylase, TNF–α, IL-1β, IL-2, and IL-6 effectively. Our study demonstrated that DCQD decreased the expression of JAM-C and MMP9 and increased the expression of AQP-1 both in vitro and in vivo. Conclusion: DCQD can reduce capillary endothelial damage in acute pancreatitis-associated intestinal injury and the mechanism may be associated with the regulation of endothelial barrier function-associated proteins AQP-1, MMP9, and JAM-C.

scholarly journals Effect of Cassave leaf flavonoid extract on TNF-α expressions in rat models suffering from periodontitis

2016 ◽  
Vol 49 (3) ◽  
pp. 137
Author(s):  
Zahara Meilawaty ◽  
Banun Kusumawardani
Keyword(s):  
Manihot Esculenta ◽  
Wistar Rats ◽  
Host Cells ◽  
Control Group ◽  
Tissue Destruction ◽  
Rat Models ◽  
Treatment Groups ◽  
E Coli ◽  
Tnf Α ◽  
Anti Inflammatory

Background: Bacteria playing a role in periodontitis are Gram-negative anaerobic bacteria that can release endotoxin or lipopolysaccharide (LPS). LPS acts as a stimulus to a variety of host cells that can stimulate expression of pro-inflammatory cytokines in periodontal disease, such as IL-1α, IL-1β, and TNF-α. Increased TNF-α then can lead to periodontal tissue destruction. Furthermore, cassava leaves have many health benefits due to flavonoid organic compound contained, known to possess anti-inflammatory activity are used as a medicine. Purpose: This study aimed to determine the effect of cassava leaf flavonoid extract as a basic ingredient of anti-inflammatory gel on TNF-α expression in Wistar rats suffering from periodontitis induced with Escherichia coli (E. coli) LPS. Method: This study used 24 male Wistar rats. Those rats were divided into six groups. Group 1 consisted of four rats induced with E. coli LPS for 2 weeks, and then decapitation was performed on day 3. Group 2 consisted of four rats induced with E. coli LPS for 2 weeks, and then decapitation was conducted on day 7. Group 3 consisted of four rats induced with E. coli LPS for 2 weeks, treated with the topical cassava leaf flavonoid extract gel (Manihot esculenta) at a concentration of 25%, and then decapitation was performed on day 3. Group 4 consisted of four rats induced with E. coli LPS for 2 weeks, treated with the topical cassava leaf flavonoid extract gel (Manihot esculenta) at a concentration of 25%, and then decapitation was conducted on day 7. Group 5 consisted of four rats induced with E. coli LPS for 2 weeks, treated with the topical cassava leaf flavonoid extract gel (Manihot esculenta) at a concentration of 50%, and then decapitation was performed on day 3. And, group 6 consisted of four rats induced with E. coli LPS for 2 weeks, treated with the topical Cassava leaf flavonoid extract gel (Manihot esculenta) at a concentration of 50%, and then decapitation was conducted on day 7. The topical Cassava leaf flavonoid extract gel was inserted into gingival sulcus on the first right molar of their lower jaw by using a blunted syringe needle. The gel was given two times a day for 7 days. Result: The expression of TNF-α in the control group was more than that in the treatment groups given the Cassava leaf flavonoid extract gel at the concentrations of 25% and 50%. The expression of TNF-α in the treatment groups given the cassava leaf flavonoid extract gel at the concentration of 50% was lower than that in the treatment groups given the cassava leaf flavonoid extract gel at the concentration of 25%. Conclusion: Cassava leaf flavonoid extract gel could be used as an anti-inflammatory gel characterized by a decrease in TNF-α expression in rat models suffering from periodontitis.

Sign in / Sign up

Export Citation Format

Share Document