Cyclosporine Ameliorates Silica-Induced Autoimmune Hepatitis in Rat Model by Altering the Expression of Toll-Like Receptor-4, Interleukin-2 and Tumor Necrosis Factor-α

2022 ◽  
Vol 22 ◽  
Author(s):  
Moustafa M. Mohamed ◽  
Ahmed M. M. Okasha ◽  
Amany H. Abdel Naiem ◽  
Reham F. Mohamed ◽  
Sayed F. Abdelwahab ◽  
...  
Keyword(s):  
Autoimmune Hepatitis ◽  
Interleukin 2 ◽  
Hepatic Function ◽  
Treated Group ◽  
Control Group ◽  
Toll Like Receptor ◽  
Hepatic Diseases ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Background: Autoimmune hepatitis (AIH) is an inflammatory liver disease which is characterized histologically by interface hepatitis, biochemically by elevated transaminase levels, and serologically by the presence of autoantibodies. Toll-like receptor (TLR)-4 is a TLR family member that, upon activation in hepatocytes, initiates a cascade of events. Interleukin-2 (IL-2) and tumour necrosis factor-α (TNF-α) are potent inflammatory cytokines secreted in AIH playing an important role in the early development of inflammation, and hepatocyte damage. Objective: This study examined cyclosporine role in AIH and tried to illustrate its actions on altered hepatic function in silica-induced AIH model. Methods: AIH was induced in Wester rats using Sodium Silicate. The rats were divided into four groups: control group, Silica-AIH group, cyclosporine-treated group, and prevention group. TLR-4, and IL-2 mRNA expression in liver tissues was tested by RT-PCR. Results: AIH was associated with up-regulation of liver enzymes, IL-2, and TLR-4 gene expression while cyclosporine significantly down-regulated the expression of both. The relative quantity of TLR-4 mRNA was 1±0, 13.57±1.91, 4±0.38, and 2±0 in the control, AIH, cyclosporine, and prevention groups, respectively (p<0.001). Also, the relative quantity of IL-2 mRNA was 1±0, 14.79±1.42, 7.07±0.96, and 3.4±0.55 in the same groups, respectively (p<0.001). Additionally, immuno-histochemical staining for TNF-α in liver sections was increased in the silica-AIH group but it was decreased in the cyclosporine-treated and prevention groups. Conclusion: This study advocates a therapeutic role of cyclosporine in treating immune-mediated hepatic diseases. Cyclosporine improves histological alterations in the liver and inhibits the production of proinflammatory cytokines.

scholarly journals Assessment of gentamicin and cisplatin-induced kidney damage mediated via necrotic and apoptosis genes in albino rats

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Tarek Kamal Abouzed ◽  
Eman Abd Elrahman Sherif ◽  
Mohamed El Sayed Barakat ◽  
Kadry Mohamed Sadek ◽  
Adil Aldhahrani ◽  
...  
Keyword(s):  
Low Cost ◽  
Treated Group ◽  
Kidney Damage ◽  
Control Group ◽  
Albino Rats ◽  
Bacterial Diseases ◽  
Tnf Α ◽  
Apoptotic Genes ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Gentamicin (GM) is a low-cost, low-resistance antibiotic commonly used to treat gram-negative bacterial diseases. Cisplatin (Csp) is a platinum-derived anti-neoplastic agent. This experiment aimed to identify the early signs of gentamicin and cisplatin-induced nephrotoxicity in rats. Thirty Wistar rats were divided into three groups of 10: a control group, which received no treatment; a gentamicin group administered by a dose of (100 mg/kg, IP) for 7 consecutive days, and a cisplatin group was administered intraperitoneal in a dose of (1.5 mg/kg body weight) repeated twice a week for 3 weeks. Results Both experimental groups exhibited increased levels of creatinine, urea, and uric acid, with the cisplatin-treated group showing higher levels than the gentamicin group. Experimental groups also exhibited significantly increased Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GSH-Px) with more pronounced effects in the cisplatin-treated group. Further, both experimental groups exhibited significant up-regulation of Tumor Necrosis Factor α (TNF-α), caspase-3, and Bax and down regulation of Bcl-2. Conclusion These findings confirm the use of necrotic, apoptotic genes as early biomarkers in the detection of tubular kidney damage. Further, cisplatin was shown to have a greater nephrotoxic effect than gentamicin; therefore, its use should be constrained accordingly when co-administered with gentamicin.

scholarly journals Assessment of Gentamicin and Cisplatin-Induced Kidney Damage Mediated via Necrotic and Apoptosis Genes in Albino Rats

2021 ◽  
Author(s):  
Mohamed El_Sayed Barakat ◽  
Tarek Kamal Abouzed ◽  
Eman Abd Elrahman Sherif ◽  
Kadry Mohamed Sadek ◽  
Adil Aldhahrani ◽  
...  
Keyword(s):  
Low Cost ◽  
Treated Group ◽  
Kidney Damage ◽  
Control Group ◽  
Albino Rats ◽  
Bacterial Diseases ◽  
Tnf Α ◽  
Apoptotic Genes ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Gentamycin (GM) is a low-cost, low-resistance antibiotic commonly used to treat gram-negative bacterial diseases. Cisplatin (Csp) is a platinum-derived anti-neoplastic agent. This experiment aimed to identify the early signs of gentamicin and cisplatin-induced nephrotoxicity in rats. 30 Wistar rats were divided into three groups of 10: a control group, which received no treatment; a gentamicin group administered by a dose of (100 mg/kg, IP) for 7 consecutive days, and a cisplatin group was administered intraperitoneal in a dose of (1.5mg/kg body weight) repeated twice a week for 3weeks. Results: Both experimental groups exhibited increased levels of creatinine, urea, and uric acid, with the cisplatin-treated group showing higher levels than the gentamicin group. Experimental groups also exhibited significantly increased malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GSH-Px) with more pronounced effects in the cisplatin-treated group. Further, both experimental groups exhibited significant up-regulation of Tumor Necrosis Factor α (TNF-α), caspase-3, and Bax and downregulation of Bcl-2. Conclusion: These findings confirm the use of necrotic, apoptotic genes as early biomarkers in the detection of tubular kidney damage. Further, cisplatin was shown to have a greater nephrotoxic effect than gentamicin; therefore, its use should be constrained accordingly when co-administered with gentamicin.

scholarly journals EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

2019 ◽  
Vol 7 (2) ◽  
pp. 66
Author(s):  
Richard Fritzgerald ◽  
Cecilia Lunardhi ◽  
Ruslan Effendy ◽  
Tamara Yuanita
Keyword(s):  
Tissue Damage ◽  
Treated Group ◽  
Positive Control ◽  
Negative Control ◽  
Control Group ◽  
Transforming Growth Factors ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction  regulator of cell growth and differentiation during reforming and remodelling.  Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth  was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry  followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of  TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

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 Application of Dexmedetomidine in Cardiopulmonary Bypass Prefilling

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582093976 ◽  
Author(s):  
Li Wang ◽  
Shaowei Wang ◽  
Zhen Xing ◽  
Fulong Li ◽  
Jinliang Teng ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Anesthesia Induction ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective: The purpose of this study was to explore the application of dexmedetomidine (Dex) in cardiopulmonary bypass. Methods: A total of 60 patients undergoing elective cardiopulmonary bypass were divided into control (C) group and Dex group. In the Dex group, appropriate amount of Dex was added into the membrane lung prefilling solution before anesthesia induction, while those in control group were given normal saline. The levels of mean arterial pressure (MAP) and heart rate (HR) at different times were measured. The levels of cardiac troponin I (CTNI), malondialdehyde (MDA), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) at different points (T0/T1/T2/T3/T4) in both groups were measured by enzyme-linked immunosorbent assay kits. Results: The intraoperative and postoperative levels of MAP and HR in the 2 groups were significantly lower than those preoperatively ( P < .05). The levels of MAP and HR in the Dex group were significantly lower than those of the C group ( P < .05). The levels of CTNI/MDA/IL-6/TNF-α at different points in both groups were significantly higher than those at T0 ( P < .05). The serum levels of CTNI, MDA, IL-6, and TNF-α in the Dex group at T1/T2/T3/T4 were significantly lower than those in the C group ( P < .05). The rate of arrhythmia in the Dex group was significantly lower than that in the C group ( P < .05). Conclusion: Dexmedetomidine has a stable effect in cardiopulmonary priming solution.

Cordyceps sinensis as an Immunomodulatory Agent

1996 ◽  
Vol 24 (02) ◽  
pp. 111-125 ◽  
Author(s):  
Yuh-Chi Kuo ◽  
Wei-Jem Tsai ◽  
Ming-Shi Shiao ◽  
Chieh-Fu Chen ◽  
Ching-Yuang Lin
Keyword(s):  
Tumor Necrosis ◽  
Nk Cell ◽  
Interleukin 2 ◽  
Cell Activity ◽  
Cordyceps Sinensis ◽  
Fruiting Bodies ◽  
Nk Cell Activity ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Effects of various fractions of methanol extracts from fruiting bodies of Cordyceps sinensis on the Iymphoproliferative response, natural killer (NK) cell activity, and phytohemagglutinin (PHA) stimulated interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α) production on human mono-nuclear cells (HMNC) were studied. Two of the 15 column fractions (CS-36-39 and CS-48-51) significantly inhibited the blastogenesis response (IC50 =; 71.0 ± 3.0 and 21.7 ± 2.0 μg/ml, respectively), NK cell activity (IC50 =; 25.0 ± 2.5 and 12.9 ± 5.8 μg/ml, respectively) and IL-2 production of HMNC stimulated by PHA (IC50 =; 9.6 ± 2.3 and 5.5 ± 1.6 μg/ml, respectively). TNF-α production in HMNC cultures was also blocked by CS-36-39 and CS-48-51 (IC50 =; 2.7 ± 1.0 and 12.5 ± 3.8 μg/ml, respectively). These results indicated that neither CS-36-39 nor CS-48-51 was cytotoxic on HMNC, and that immunosuppressive ingredients are contained in Cordyceps sinensis.

scholarly journals TINGGINYA KADAR TUMOR NECROSIS FACTOR-α (TNF-α) PLASMA PADA MENCIT BUNTING YANG TERINFEKSI PLASMODIUM BERGHEI BERHUBUNGAN KUAT DENGAN KADAR HEMOGLOBIN YANG RENDAH TETAPI TIDAK BERHUBUNGAN DENGAN BERAT BADAN JANIN RENDAH

2013 ◽  
Vol 2 (1) ◽  
pp. 51-64
Author(s):  
Yuliyanik Yuliyanik
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Placental Tissue ◽  
Control Group ◽  
Study Group ◽  
Low Weight ◽  
Tnf Α ◽  
Pregnant Mice ◽  
Factor Α ◽  
Necrosis Factor

Malaria infection in pregnancy may increase the morbidity and mortality of both mother and fetus. In pregnant women, it can lead to severe anemia, cerebral malaria, pulmonary edema, renal failure and even death, while in the fetus it can cause abortion, premature birth, low birth weight, and fetal death. Elevated levels of tumor necrosis factor-α(TNF-α ) is associated with low birth weight and anemia in pregnant women. This study was conducted to measure the levels of TNF-α in plasma and placental tissue, and hemoglobin levels as well as fetal weight to determine the relationship between them in P. berghei infected pregnant mice and normal pregnant mice. Seventeen BALB/c mice used in this study were divided into two groups, those were the study group (9 pregnant mice infected with P. berghei) and control group (8 pregnant mice not infected with P. berghei). Level of TNF-α were measured using Enzyme Linked Immunosorbent assay (R&D Systems, catalog A00B MT). Hemoglobin levels were determined using flowcytometri, whereas fetal weight were performed with Mettler analytical balance AE 50. T-test statistical analysis showed that the levels of TNF-α in plasma and placental tissue in study group were higher than control group (p=0.000, p=0.034). Hemoglobin levels in the study group were lower than control group (p=0.025). Fetal weights were also lower in fetuses of infected mice than fetuses of uninfected mice (p=0.002). Pearson correlation test showed increasing plasma levels of TNF-α in infected P. berghei pregnant mice were related with the decreasing levels of Hb, (r=-0.748; p=0.020,), whereas levels of placental TNF-α were not associated with hemoglobin level (p=0.337). Both plasma and placental levels of TNF-α were not associated with the incidence of fetal low weight (p=0.380, and p=0.365). It can be concluded that the increased levels of TNF-α is associated with decreased levels of hemoglobin (Hb), but not associated with fetal low weight.

scholarly journals Postoperative Effects of Dexmedetomidine on Serum Inflammatory Factors and Cognitive Malfunctioning in Patients with General Anesthesia

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Zitan Zhang ◽  
Wei Li ◽  
Huiqun Jia
Keyword(s):  
Elderly Patients ◽  
General Anesthesia ◽  
Postoperative Cognitive Dysfunction ◽  
Inflammatory Factors ◽  
Control Group ◽  
Inflammatory Factor ◽  
Tnf Α ◽  
Random Number Table ◽  
Factor Α ◽  
Necrosis Factor

Objective. To investigate the effects of dexmedetomidine intervention on serum inflammatory factor concentration and postoperative cognitive malfunction in elderly patients with general anesthesia. Methodology. 174 patients with general anesthesia were selected, who were categorized into a control group (HC) and a dexmedetomidine group (HS) using the random number table method, with 87 patients in individual groups. The dexmedetomidine group was pumped intravenously with dexmedetomidine at a loading dose of 1 μg/kg before induction of anesthesia for 15 min, followed by continuous intravenous pumping at a rate of 0.4 μg/kg/h, and the dosing was stopped at 30 min before concluding the surgery. The control group was administered the identical dose of saline in the same manner. Interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) levels and MMES scores were tested at 1 h before and 24 h after anesthesia. Results. Comparing to HC group, patients in the HS group had lower TNF-α and IL-6 levels at both scheduled points ( P  < 0.05). Conclusion. Dexmedetomidine reduced the expression of inflammatory factors in elderly patients with general anesthesia and effectively reduced the incidence of postoperative cognitive dysfunction after general anesthesia surgery.

Effect of Hypothermia on Serum Myelin Basic Protein and Tumor Necrosis Factor-α in Neonatal Hypoxic-Ischemic Encephalopathy

2021 ◽  
Author(s):  
Qiuli Wang ◽  
Hongyan Lv ◽  
Sujing Wu ◽  
Junxia Song ◽  
Junqin Li ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Basic Protein ◽  
Serum Levels ◽  
Control Group ◽  
Tnf Α ◽  
Hypothermia Group ◽  
Neurodevelopmental Impairment ◽  
Factor Α ◽  
Ischemic Encephalopathy ◽  
Necrosis Factor

Objective Multiple randomized controlled trials have shown that hypothermia is a safe and effective treatment for neonatal moderate or severe hypoxic-ischemic encephalopathy (HIE). The neuroprotective mechanisms of hypothermia need further study. The aim of this study was to investigate the effect of hypothermia on the serum levels of myelin basic protein (MBP) and tumor necrosis factor-α (TNF-α) as well as neurodevelopmental outcomes in neonatal HIE. Study Design Eighty-five neonates with moderate-to-severe HIE were divided into a hypothermia group (n = 49) and a control group (n = 36). Serum levels of MBP and TNF-α within 6 hours after birth and after 3 days of treatment were determined by enzyme-linked immunosorbent assay, and neurodevelopmental outcome at the age of 12 to 15 months was assessed by using the Gesell development scale. Results After 3 days of treatment, serum levels of MBP and TNF-α in the control group were not significantly different from levels before treatment (p > 0.05), and serum levels of MBP and TNF-α in the hypothermia group were significantly lower than levels before treatment (p < 0.05). Serum levels of MBP and TNF-α were significantly negatively correlated with developmental quotient (DQ; r =  − 0.7945, p = 0.0000; r =  − 0.7035, p = 0.0000, respectively). Serum levels of MBP and TNF-α in neurodevelopmentally impaired infants were significantly higher than those in infants with suspected neurodevelopmental impairment and those in neurodevelopmentally normal infants (both p < 0.01). The rate of reduction of neurodevelopmental impairment was higher among infants in the hypothermia group than among those in the control group (χ2 = 16.3900, p < 0.05). Conclusion Hypothermia can reduce serum levels of MBP and TNF-α in neonates with HIE. Inhibiting the release of TNF-α may be one of the mechanisms by which hypothermia protects the myelin sheath. Key Points

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