scholarly journals Aqueous extract of Kan-Lu-Hsiao-Tu-Tan ameliorates collagen-induced arthritis in mice by regulating immune and inflammatory responses

2020 ◽  
Author(s):  
Chih-Chao Chiang ◽  
Yi‐Rong Li ◽  
Kuei-Hung Lai ◽  
Wei-Jen Cheng ◽  
Shih-Chao Lin ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Inflammatory Responses ◽  
Thiobarbituric Acid ◽  
Therapeutic Effects ◽  
Inflammatory Disorder ◽  
Splenocyte Proliferation ◽  
Thiobarbituric Acid Reactive Substances ◽  
Collagen Induced Arthritis ◽  
Factor Α ◽  
Necrosis Factor

Abstract Abstract: Background: Kan-Lu-Hsiao-Tu-Tan (KLHTT) exhibits anti-psoriatic effects through anti-inflammatory activity in mice. However, the therapeutic effects of KLHTT on rheumatoid arthritis (RA), another significant autoimmune inflammatory disorder, are not elucidated. Herein, we explored the anti-arthritic effects of KLHTT on collagen-induced arthritis (CIA) in mice. Methods: KLHTT was extracted by boiling water and subjected to spectroscopic analysis. Chicken collagen type II (CII) with complete Freund’s adjuvant was intradermally injected to induce CIA in DBA/1J mice. Anti-CII antibody, cytokines, malondialdehyde (MDA), and hydrogen peroxide (H2O2) were measured using ELISA, thiobarbituric acid reactive substances, and hydrogen peroxide assay kit. Splenocyte proliferation was tested using thymidine incorporation. Th1 and Th17 cells were analyzed by flow cytometry. Results: Oral KLHTT treatment (50 and 100 mg/kg) ameliorated mouse CIA by decreasing the levels of interleukin (IL)-1β, IL-6, IL-17A, and tumour necrosis factor-α in the paw homogenates and serum. KLHTT also suppressed anti-CII antibody formation, splenocyte proliferation, and splenic Th1 and Th17 cell numbers. Additionally, KLHTT showed antioxidant activity by reducing the concentrations of MDA and H2O2 in paw tissues. Conclusions: The therapeutic effects of KLHTT in CIA mice were through regulating oxidative stress and inflammatory responses. Our results suggest that KLHTT has potential to treat RA.

scholarly journals Aqueous Extract of Kan-Lu-Hsiao-Tu-Tan Ameliorates Collagen-Induced Arthritis in Mice by Inhibiting Oxidative Stress and Inflammatory Responses

Life ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 313
Author(s):  
Chih-Chao Chiang ◽  
Yi-Rong Li ◽  
Kuei-Hung Lai ◽  
Wei-Jen Cheng ◽  
Shih-Chao Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Inflammatory Responses ◽  
Thiobarbituric Acid ◽  
Therapeutic Effects ◽  
Inflammatory Disorder ◽  
Splenocyte Proliferation ◽  
Collagen Induced Arthritis ◽  
Factor Α ◽  
Necrosis Factor

Background: Kan-Lu-Hsiao-Tu-Tan (KLHTT) exhibits anti-psoriatic effects through anti-inflammatory activity in mice. However, the therapeutic effects of KLHTT on rheumatoid arthritis (RA), another significant autoimmune inflammatory disorder, have not been elucidated. Herein, we explored the anti-arthritic effects of KLHTT on collagen-induced arthritis (CIA) in mice. Methods: KLHTT was extracted by boiling water and subjected to spectroscopic analysis. Chicken collagen type II (CII) with complete Freund’s adjuvant was intradermally injected to induce CIA in DBA/1J mice. Anti-CII antibody, cytokines, malondialdehyde (MDA), and hydrogen peroxide (H2O2) were measured using ELISA, thiobarbituric acid reactive substances, and a hydrogen peroxide assay kit. Splenocyte proliferation was tested using thymidine incorporation. Th1 and Th17 cells were analyzed by flow cytometry. Results: Oral KLHTT treatment (50 and 100 mg/kg) ameliorated mouse CIA by decreasing the levels of interleukin (IL)-1β, IL-6, IL-17A, and tumour necrosis factor-α in the paw homogenates and serum. KLHTT also suppressed anti-CII antibody formation, splenocyte proliferation, and splenic Th1 and Th17 cell numbers. Additionally, KLHTT showed antioxidant activity by reducing the concentrations of MDA and H2O2 in paw tissues. Conclusions: The therapeutic effects of KLHTT in CIA mice were through regulating oxidative stress and inflammatory responses. Our results suggest that KLHTT has potential to treat RA.

Remote myocardial injury: the protective role of fluoxetine

2018 ◽  
Vol 96 (4) ◽  
pp. 319-327 ◽  
Author(s):  
Onur M. Yaman ◽  
Hayriye Erman ◽  
Ibrahim Guner ◽  
Olgu Enis Tok ◽  
Mukaddes Pala ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Cardiac Injury ◽  
Lipid Hydroperoxide ◽  
Thiobarbituric Acid ◽  
Interleukin 10 ◽  
Myeloperoxidase Activity ◽  
Thiobarbituric Acid Reactive Substances ◽  
Anti Oxidant ◽  
Factor Α ◽  
Necrosis Factor

Aortic cross-clamping-induced ischemia–reperfusion (IR) is an important factor in the development of postoperative acute cardiac injury following abdominal aortic surgery. We investigated the possible anti-oxidant/anti-inflammatory effects of fluoxetine (FLX), which is used widely as a preoperative anxiolytic on cardiac injury induced by IR of the infrarenal abdominal aorta. FLX was administered to IR-performed (60 min of ischemia and 120 min of reperfusion) rats for 3 days, once daily at 20 mg/kg i.p. dosage. Results were compared to control and non-FLX-treated IR-performed rats. Serum creatine kinase (CK) and CK-MB levels, lipid hydroperoxide, thiobarbituric acid reactive substances, and pro-oxidant/anti-oxidant balance levels in the IR group were significantly higher whereas superoxide dismutase activity, glutathione, and ferric reducing/anti-oxidant power levels were lower than for the control. IR also increased myeloperoxidase activity, tumor necrosis factor-α, interleukin-1β, and interleukin-6 and decreased interleukin-10 levels. FLX decreased CK, CK-MB, lipid hydroperoxide, thiobarbituric acid reactive substances, and pro-oxidant/anti-oxidant balance levels while increasing superoxide dismutase activity, glutathione, and ferric reducing/anti-oxidant power levels. FLX also decreased myeloperoxidase activity, tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels and increased interleukin-10 levels compared to IR. FLX attenuated the morphological changes associated with cardiac injury. Our study clearly demonstrates that FLX confers protection against aortic IR-induced cardiac injury, tissue leucocyte infiltration, and cellular integrity via its anti-oxidant/anti-inflammatory effects.

scholarly journals Orientin Attenuates Cisplatin-Induced Renal Toxicity by Reducing Oxidative Stress and Inflammation

2021 ◽  
Vol 41 (04) ◽  
pp. 574-578
Author(s):  
Muhammad Umar Ijaz
Keyword(s):  
Renal Damage ◽  
Renal Toxicity ◽  
Thiobarbituric Acid ◽  
Protective Role ◽  
Male Rats ◽  
Thiobarbituric Acid Reactive Substances ◽  
Catalase Peroxidase ◽  
Factor Α ◽  
Therapeutic Activities ◽  
Necrosis Factor

Cisplatin (CP), an effective chemotherapeutic drug, has been widely used to treat the several types of tumors. Orientin (ORI) is a flavonoid that shows versatile therapeutic activities. The current research was planned to observe the protective role ORI on CP induced renal injury in rats. Twenty-four male rats were divided into four groups equally and termed as control, CP (10 mg/kg), CP (10 mg/kg) + ORI (40 mg/kg) and ORI (40 mg/kg). After seven days trial, rats were dissected and different parameters were analyzed. Results indicated that the CP administration significantly reduced the activities of catalase, peroxidase, glutathione reductase and glutathione content whereas it increased the level of hydrogen peroxide and TBARS (thiobarbituric acid reactive substances). CP increased the creatinine and urea levels while decreased the creatinine clearance. Moreover, CP significantly increased the inflammatory markers, including nuclear factor kappa-B, tumor necrosis factor-α, Interleukin-6, Interleukin-1β levels, cyclooxygenase-2 activity and histopathological damages. However, co-administration of ORI displayed curative effects against CP-induced renal toxicity and recovered all parameters by bringing them to a normal level. These results revealed that the ORI is a potential bioflavonoid that can potentially counter the CP-induced renal damage.

scholarly journals Melatonin Regulates Oxidative Stress Initiated by Freund’s Complete Adjuvant

2015 ◽  
Vol 58 (1) ◽  
pp. 21-24 ◽  
Author(s):  
Miroslav Pohanka ◽  
Branislav Ruttkay-Nedecký ◽  
Josef Fusek ◽  
Vojtěch Adam ◽  
René Kizek
Keyword(s):  
Tumor Necrosis Factor ◽  
Glutathione Reductase ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Freund’S Complete Adjuvant ◽  
Freund's Complete Adjuvant ◽  
Factor Α ◽  
Necrosis Factor

Melatonin is a hormone with strong antioxidant properties. In this experiment, Freund’s complete adjuvant was used as a stressogenic substance given to laboratory outbred mice, whereas melatonin was investigated as a protectant against the stressogenic effect. Levels of low molecular weight antioxidants, thiobarbituric acid reactive substances, and tumor necrosis factor α and activity of glutathione reductase were determined in blood from the animals. Surprisingly, melatonin was not involved in direct regulation of antioxidants, thiobarbituric acid reactive substances and tumor necrosis factor α. On the other hand, melatonin regulated glutathione reductase activity. We can conclude on regulation of metabolism caused by melatonin in the model. The effect was more important than the expected regulation of immunity and basal oxidative homeostasis.

scholarly journals Aqueous extract of Kan-Lu-Hsiao-Tu-Tan ameliorates collagen-induced arthritis in mice by regulating immune and inflammatory responses

2020 ◽  
Author(s):  
Chih-Chao Chiang ◽  
Yi‐Rong Li ◽  
Kuei-Hung Lai ◽  
Wei-Jen Cheng ◽  
Shih-Chao Lin ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Hydrogen Peroxide ◽  
Th17 Cells ◽  
Inflammatory Responses ◽  
Bone Erosion ◽  
Cartilage Damage ◽  
Radical Scavenging ◽  
Therapeutic Effects ◽  
Collagen Induced Arthritis ◽  
Anti Inflammatory

Abstract Background Rheumatoid arthritis (RA) is an autoimmune disease featured by joint inflammation and systemic comorbidities. Kan-Lu-Hsiao-Tu-Tan (KLHTT), a Chinese medicine formulation, has free radical scavenging capacity and anti-inflammatory activity in vitro. However, its anti-arthritic effect remains unknown. Herein, we aimed to explore the anti-arthritic effects of KLHTT on collagen-induced arthritis (CIA) in mice and investigate the underlying mechanisms. Methods KLHTT was extracted using boiling water. KLHTT (50 and 100 mg/kg) was fed orally for 21 days once a day on CIA in DBA/1J mice. The severity of CIA was evaluated by histological assessments. Levels of inflammatory cytokines, malondialdehyde (MDA), and hydrogen peroxide (H2O2) were measured using ELISA, thiobarbituric acid reactive substances, and hydrogen peroxide assay kits, respectively. Anti-collagen type II (CII) antibody was assayed by ELISA. Proliferation of splenocytes was tested using radioactive thymidine incorporation assay. Levels of Th1 and Th17 cells were obtained using flow cytometry. Results KLHTT significantly ameliorated paw edema and restored body weight in CIA mice. The synovitis, cartilage damage, and bone erosion were reduced by KLHTT. KLHTT exhibited anti-inflammatory effects by decreasing the levels of interleukin (IL)-1β, IL-6, IL-17A, and tumour necrosis factor-α in the paw homogenates and serum. KLHTT also showed antioxidant activity by reducing the concentrations of MDA and H2O2 in paw tissues. Moreover, KLHTT reduced anti-CII antibody formation, suppressed splenocyte proliferation, and mitigated the levels of splenic Th1 and Th17 cells in CIA mice. Conclusion The therapeutic effects of KLHTT in CIA mice were through regulating immune and inflammatory responses. Our results suggest that KLHTT has potential to treat rheumatoid arthritis.

scholarly journals SAT0007 BLOCKING HISTAMINE-RELEASING FACTOR/TRANSLATIONALLY CONTROLLED TUMOR PROTEIN (HRF/TCTP) ATTENUATES AGGRESSIVENESS OF FIBROBLAST-LIKE SYNOVIOCYTES AND AMELIORATES COLLAGEN-INDUCED ARTHRITIS IN RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 934.3-934
Author(s):  
M. Kim ◽  
Y. Choe ◽  
H. Lee ◽  
Y. H. Cheon ◽  
S. I. Lee
Keyword(s):  
Rheumatoid Arthritis ◽  
Cancer Progression ◽  
Inflammatory Responses ◽  
Joint Destruction ◽  
Serum Levels ◽  
Therapeutic Effects ◽  
Collagen Induced Arthritis ◽  
Translationally Controlled Tumor Protein ◽  
Biochemical Analyses ◽  
Fibroblast Like Synoviocytes

Background:Histamine-releasing factor/translationally controlled tumor protein (HRF/TCTP) stimulates cancer progression and allergic responses. Increased expression of HRF/TCTP occurs in joints of rheumatoid arthritis (RA) patients, but the role of HRF/TCTP in RA remains undefinedObjectives:In this study, we explored the pathogenic significance of HRF/TCTP and evaluated therapeutic effects of HRF/TCTP blockade in RA.Methods:HRF/TCTP transgenic (TG) and knockdown (KD) mice with collagen-induced arthritis (CIA) were used to determine experimental phenotypes of RA. HRF/TCTP levels were measured in sera and joint fluids in patients with RA and compared to those with osteoarthritis, ankylosing spondylitis, Behcet disease, and healthy controls. HRF/TCTP expression was also assessed in synovium and fibroblast-like synoviocytes (FLS) obtained from RA or OA patients. Finally, we assessed effects of HRF/TCTP and dimerized HRF/TCTP binding peptide-2 (dTBP2), an inhibitor of HRF/TCTP, in RA-FLS and CIA mice.Results:Our clinical, radiological, histological, and biochemical analyses indicate that inflammatory responses and joint destruction were increased in HRF/TCTP TG mice, and decreased in KD mice compared to wild-type littermates. HRF/TCTP levels were higher in sera, synovial fluid, synovium, and FLS of patients with RA than in control groups. Serum levels of HRF/TCTP correlated well with disease activity in RA. Tumor-like aggressiveness of RA-FLS was exacerbated by HRF/TCTP stimulation and ameliorated by dTBP2 treatment. dTBP2 exerted protective and therapeutic effects in CIA mice, and had no detrimental effect in a murine tuberculosis model.Conclusion:Our results indicate that HRF/TCTP represents a novel biomarker and therapeutic target for diagnosis and treatment of RA.References:N/AAcknowledgments :National Research Foundation of KoreaKorea Health Industry Development InstituteDisclosure of Interests:None declared

scholarly journals Mammalian Peroxiredoxin Isoforms Can Reduce Hydrogen Peroxide Generated in Response to Growth Factors and Tumor Necrosis Factor-α

1998 ◽  
Vol 273 (11) ◽  
pp. 6297-6302 ◽  
Author(s):  
Sang Won Kang ◽  
Ho Zoon Chae ◽  
Min Seok Seo ◽  
Kanghwa Kim ◽  
Ivan C. Baines ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Growth Factors ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Lipopolysaccharide induces neuroglia activation and NF-κB activation in cerebral cortex of adult mice

2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Ju-Bin Kang ◽  
Dong-Ju Park ◽  
Murad-Ali Shah ◽  
Myeong-Ok Kim ◽  
Phil-Ok Koh
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Calcium Binding ◽  
Inflammatory Responses ◽  
Inflammatory Factors ◽  
Adult Mice ◽  
Tnf Α ◽  
Factor Α ◽  
And Oxidative Stress ◽  
Necrosis Factor

Abstract Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 μg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.

scholarly journals Spirulina maxima and its effect on antioxidant activity in fructose induced oxidative stress with histopathological observations

2015 ◽  
Vol 62 (2) ◽  
pp. 13-19
Author(s):  
Urmila Jarouliya ◽  
Anish Zacharia ◽  
Raj K. Keservani ◽  
Godavarthi B.K.S Prasad
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Superoxide Dismutase ◽  
Blood Glucose ◽  
Reduced Glutathione ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Therapeutic Effects ◽  
Thiobarbituric Acid Reactive Substances ◽  
Spirulina Maxima

Abstract Diabetes mellitus is a metabolic disorder characterised by hyperglycemia and oxidative stress. The aim of the present study is to explore the antioxidant effect of Spirulina maxima in rat model along with the histopathological observations. Diabetes was induced by feeding 10% fructose solution orally to Wistar rats (n = 6) for 30 days, analysed for plasma blood glucose and the markers of the oxidative stress [catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS)]. These biochemical studies were associated with histopathological examination of liver and kidney sections. The microalga Spirulina maxima being rich in proteins and other essential nutrients is widely used as a food supplement. S. maxima at a dose of 5 and 10% per kg and the metformin (500 mg/kg) as reference drug were given orally for 30 days to the diabetic rats. Diabetic rats showed significant (p < 0.001) elevations in plasma blood glucose, thiobarbituric acid-reactive substances and significant reduction in catalase, superoxide dismutase and reduced glutathione activity. Oral administration of 5 and 10% aqueous extract of S. maxima for 30 days restored not only of blood glucose levels but also markers of oxidative stress. Histopathological observations of tissues manifested that the S. maxima administration had the protective and therapeutic effects against fructose-induced abnormalities in diabetic rats. It is concluded that S. maxima is effective in reinstating the antioxidant activity in addition to its antidiabetic effect in type 2 diabetic rats.

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