scholarly journals Anti-Inflammation Effect of Small Molecule Oligopeptides Prepared from Panax ginseng C. A. Meyer in Rats

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 858 ◽  
Author(s):  
Meihong Xu ◽  
Qihe Chen ◽  
Rui Fan ◽  
Junbo Wang ◽  
Yong Li
Keyword(s):  
Platelet Activating Factor ◽  
Sprague Dawley ◽  
Edema Formation ◽  
Leukotriene D4 ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
G 12 ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Acute And Chronic Inflammation

The present study was designed to investigate the anti-inflammatory effects of ginseng oligopeptides (GOPs). For the anti-inflammatory activity, dextran-induced paw edema and granuloma models were used in Sprague-Dawley rats (180–200 g, 12 weeks old, n = 10). Rats were treated orally with GOPs (0, 62.5, 125, 250 and 500 mg/kg) for prophylaxis. In the granuloma model, the levels of NO, Tumor necrosis factor-α (TNF-α), interleukin IL-β, and interleukin IL-10 in serum were evaluated. In addition, in the edema model, the level of TNF-α, prostaglandin E2 (PGE2), Leukotriene D4 (LTD4), and the platelet activating factor (RAF) in paw tissue were detected. PCR assessed the effect of GOPs on the expression of MAPK and NF-κB. The results showed that oral administration of GOPs inhibited inflammation caused by cotton pellet and dextran. GOPs significantly inhibited the edema formation via MAPK and NF-κB. These findings suggested that GOPs have a beneficial effect on acute and chronic inflammation, and the mechanism possibly mediated by inhibiting gene expression involved in inflammation and downregulating inflammatory mediators.

scholarly journals The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2020 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Acrylamide (ACR) formed during heating of tobacco and carbohydrate-rich food as well as widely applied in industries has been known as a well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats.Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the cerebral homogenates were detected using ELISA assay.Results: ACR-induced weigh loss, deficits in motor function as well as pathological alterations in brains were significantly improved in rats administrated with 50 and 100 mg/kg curcumin. TUNEL-positive apoptotic cells in curcumin-treated ACR intoxicated brains were less than those in the ACR model group. Curcumin administration especially at the dose of 100 mg/kg upregulated the TERT mRNA expression and enhanced the number of TERT-positive cells in ACR-intoxicated cortex tissues. Moreover, curcumin treatment reduced the concentrations of TNF-α, IL-1β and MDA, while increased the GSH contents as well as the SOD and GSH-Px activities in the cerebral homogenates, in comparison to ACR control group.Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. Maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

scholarly journals Anti-inflammatory activity of palmitoylethanolamide ameliorates osteoarthritis induced by monosodium iodoacetate in Sprague–Dawley rats

2021 ◽  
Vol 29 (5) ◽  
pp. 1475-1486
Author(s):  
Jae In Jung ◽  
Hyun Sook Lee ◽  
Young Eun Jeon ◽  
So Mi Kim ◽  
Su Hee Hong ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Acid Amide ◽  
Treatment Strategies ◽  
Leukotriene B4 ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Monosodium Iodoacetate ◽  
Anti Inflammatory

AbstractNovel treatment strategies are urgently required for osteoarthritis (OA). Palmitoylethanolamide (PEA) is a naturally occurring fatty acid amide with analgesic and anti-inflammatory effects. We aimed to examine its effect on OA and elucidate the molecular mechanism of actions in monosodium iodoacetate (MIA)-induced OA Sprague–Dawley rats. The experimental animals were divided into normal control group (injected with saline + treated with phosphate-buffered saline (PBS), NOR), control group (injected with MIA + treated with PBS, CON), 50 or 100 mg/kg body weight (BW)/day PEA-treated group (injected with MIA + treated with 50 or 100 mg of PEA/kg BW/day, PEA50 or PEA100), and positive control group (injected with MIA + treated with 6 mg of diclofenac/kg BW/day, DiC). The changes in blood parameters, body parameters, gene expression of inflammatory mediators and cytokines, knee thickness, and joint tissue were observed. Oral administration of PEA had no adverse effects on the BW, liver, or kidneys. PEA reduced knee joint swelling and cartilage degradation in MIA-induced OA rats. The serum levels of leukotriene B4, nitric oxide, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and prostaglandin E2 considerably reduced in the PEA100 group compared with those in the CON group. In the synovia of knee joints, the mRNA expression of iNOS, 5-Lox, Cox-2, Il-1β, Tnf-α, and Mmp-2, -3, -9, and -13 apparently increased with MIA administration. Meanwhile, Timp-1 mRNA expression apparently decreased in the CON group but increased to the normal level with PEA treatment. Thus, PEA can be an effective therapeutic agent for OA.

The time course of inflammatory cytokine secretion in a rat model of postoperative pain does not coincide with the onset of mechanical hyperalgesia

2007 ◽  
Vol 85 (6) ◽  
pp. 613-620 ◽  
Author(s):  
Lisa C. Loram ◽  
Andreas C. Themistocleous ◽  
Linda G. Fick ◽  
Peter R. Kamerman
Keyword(s):  
Postoperative Pain ◽  
Inflammatory Cytokine ◽  
Time Course ◽  
Mechanical Stimulus ◽  
Sprague Dawley ◽  
Tissue Samples ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Primary Hyperalgesia ◽  
Factor Α

We characterized the time course of inflammatory cytokine release at the site of injury and in plasma after surgery on the rat tail. Anesthetized Sprague–Dawley rats had a 20 mm long incision made through the skin and fascia of their tails. Control rats were anesthetized, but no incision was made. Blood and tissue samples were taken 2 h and 1, 2, 4, and 8 days after surgery and analysed by ELISA for interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and cytokine-induced neutrophil chemoattractant-1 (CINC-1). In another group of rats, daily behavioral measurements were made of the rats’ responses to a blunt noxious mechanical stimulus (4 Newtons) applied to their tails. Primary hyperalgesia developed within 2 h of surgery and lasted for 6 days. The tissue concentrations of IL-1β, IL-6, and CINC-1 increased within 24 h of surgery, and TNF-α concentration increased within 48 h of surgery. Thereafter, cytokine concentrations remained elevated for 4 (IL-1β and IL-6) to 8 days (CINC-1, TNF-α) after surgery. Control animals did not develop hyperalgesia and no changes in cytokines concentrations were detected. Thus, in our model of postoperative pain, secretion of inflammatory cytokines IL-1β, IL-6, TNF-α, and CINC-1 was not essential for the initiation of postoperative hyperalgesia.

scholarly journals Spinal NMDA receptor activation constrains inactivity-induced phrenic motor facilitation in Charles River Sprague-Dawley rats

2014 ◽  
Vol 117 (7) ◽  
pp. 682-693 ◽  
Author(s):  
K. A. Streeter ◽  
T. L. Baker-Herman
Keyword(s):  
Motor Neurons ◽  
Neural Activity ◽  
Receptor Activation ◽  
Motor Nucleus ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Burst Amplitude ◽  
Nmdar Activation ◽  
Factor Α

Reduced spinal synaptic inputs to phrenic motor neurons elicit a unique form of spinal plasticity known as inactivity-induced phrenic motor facilitation (iPMF). iPMF requires tumor necrosis factor-α (TNF-α) and atypical protein kinase C (aPKC) activity within spinal segments containing the phrenic motor nucleus to stabilize early, transient increases in phrenic burst amplitude into long-lasting iPMF. Here we tested the hypothesis that spinal N-methyl-d-aspartate receptor (NMDAR) activation constrains long-lasting iPMF in some rat substrains. Phrenic motor output was recorded in anesthetized, ventilated Harlan (HSD) and Charles River (CRSD) Sprague-Dawley rats exposed to a 30-min central neural apnea. HSD rats expressed a robust, long-lasting (>60 min) increase in phrenic burst amplitude (i.e., long-lasting iPMF) when respiratory neural activity was restored. By contrast, CRSD rats expressed an attenuated, transient (∼15 min) iPMF. Spinal NMDAR inhibition with DL-2-amino-5-phosphonopentanoic acid (APV) before neural apnea or shortly (4 min) prior to the resumption of respiratory neural activity revealed long-lasting iPMF in CRSD rats that was phenotypically similar to that in HSD rats. By contrast, APV did not alter iPMF expression in HSD rats. Spinal TNF-α or aPKC inhibition impaired long-lasting iPMF enabled by NMDAR inhibition in CRSD rats, suggesting that similar mechanisms give rise to long-lasting iPMF in CRSD rats with NMDAR inhibition as those giving rise to long-lasting iPMF in HSD rats. These results suggest that NMDAR activation can impose constraints on TNF-α-induced aPKC activation after neural apnea, impairing stabilization of transient iPMF into long-lasting iPMF. These data may have important implications for understanding differential responses to reduced respiratory neural activity in a heterogeneous human population.

scholarly journals The Anti-Inflammatory Activity of Palmitoylethanolamide Ameliorates Osteoarthritis Induced by Monosodium Iodoacetate in Sprague Dawley Rats

2021 ◽  
Author(s):  
Jae In Jung ◽  
Hyun Sook Lee ◽  
Young Eun Jeon ◽  
So Mi Kim ◽  
Su Hee Hong ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Acid Amide ◽  
Leukotriene B4 ◽  
Joint Disease ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Monosodium Iodoacetate ◽  
Anti Inflammatory

Abstract Novel treatment strategies are urgently required for osteoarthritis (OA), a degenerative joint disease. Palmitoylethanolamide (PEA) is a naturally occurring fatty acid amide with analgesic and anti-inflammatory effects. We aimed to examine its effect on OA and molecular mechanism of actions in monosodium iodoacetate (MIA)-induced OA Sprague Dawley rats. The experimental animals were divided into five groups: normal control group (injected with saline + treated with phosphate-buffered saline (PBS), NOR), control group (injected with MIA + treated with PBS, CON), 50 or 100 mg/kg body weight (BW)/day PEA-treated group (injected with MIA + treated with 50 or 100 mg of PEA/kg BW/day, PEA50 or PEA 100), and positive control group (injected with MIA + treated with 6 mg of diclofenac/kg BW/day, DiC). Changes in blood and body parameters, gene expression of inflammatory mediators and cytokines, knee thickness, and joint tissue were observed. We found no adverse effects of oral administration of PEA on BW, liver, or kidneys. PEA reduced knee joint swelling and cartilage degradation in MIA-induced OA rats. The serum levels of leukotriene B4, nitric oxide, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and prostaglandin E2 considerably reduced in the PEA100 group compared to those in the CON group. In the synovia of knee joints, mRNA expression of iNOS, 5-Lox, Cox-2, Il-1β, Tnf-α, Mmp-2, -3, -9, and − 13 noticeably reduced with MIA administration. Meanwhile, Timp-1 mRNA expression noticeably decreased in the CON group but increased to the normal level with PEA treatment. Thus, we demonstrated that PEA can be used as an effective therapeutic agent for OA.

Curcumin and Saikosaponin A Inhibit Chemical-Induced Liver Inflammation and Fibrosis in Rats

2010 ◽  
Vol 38 (01) ◽  
pp. 99-111 ◽  
Author(s):  
Shu-Ju Wu ◽  
Ka-Wai Tam ◽  
Ya-Hui Tsai ◽  
Chun-Chao Chang ◽  
Jane C.-J. Chao
Keyword(s):  
Transforming Growth Factor ◽  
Interleukin 10 ◽  
Transforming Growth Factor Β1 ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Histopathological Results ◽  
Necrosis Factor ◽  
Saikosaponin A

Curcumin and saikosaponin A as antioxidants improve antioxidant status. This study investigated the anti-inflammatory and antifibrotic actions of curcumin and saikosaponin A on CCl4 -induced liver damage. Sprague-Dawley rats were randomly divided into control, CCl4 , CCl4+ curcumin (0.005%; CU), CCl4 + saikosaponin A (0.004%; SS), and CCl4 + curcumin + saikosaponin A (0.005% + 0.004%; CU + SS) groups. Carbon tetrachloride (40% in olive oil) at a dose of 0.75 ml/kg was injected intraperitoneally once a week. Curcumin and saikosaponin A were supplemented alone or in combination with diet 1 week before CCl4 injection for 8 weeks. After 8-week supplementation, histopathological results showed hepatic collagen deposition was significantly reduced in the CU and SS groups, and activated nuclear factor-κ B expression induced by CCl4 in the liver was significantly inhibited by curcumin and/or saikosaponin A. Hepatic proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 were significantly inhibited, and anti-inflammatory cytokine interleukin-10 was significantly increased by supplementation with curcumin and/or saikosaponin A. Additionally, curcumin and/or saikosaponin A significantly reduced the increased levels of hepatic transforming growth factor-β1 and hydroxyproline after CCl4 treatment. Therefore, supplementation with curcumin and/or saikosaponin A suppress inflammation and fibrogenesis in rats with CCl4 -induced liver injury. However, the combination has no additive effects on anti-inflammation and antifibrosis.

scholarly journals TNF-α-Mediated RIPK1 Pathway Participates in the Development of Trigeminal Neuropathic Pain in Rats

2022 ◽  
Vol 23 (1) ◽  
pp. 506
Author(s):  
Jo Young Son ◽  
Jin Sook Ju ◽  
Yu Mi Kim ◽  
Dong Kuk Ahn
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Mechanical Allodynia ◽  
Inflammatory Responses ◽  
Inferior Alveolar Nerve ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Factor Α ◽  
Inferior Alveolar Nerve Injury

Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) participates in the regulation of cellular stress and inflammatory responses, but its function in neuropathic pain remains poorly understood. This study evaluated the role of RIPK1 in neuropathic pain following inferior alveolar nerve injury. We developed a model using malpositioned dental implants in male Sprague Dawley rats. This model resulted in significant mechanical allodynia and upregulated RIPK1 expression in the trigeminal subnucleus caudalis (TSC). The intracisternal administration of Necrosatin-1 (Nec-1), an RIPK1 inhibitor, blocked the mechanical allodynia produced by inferior alveolar nerve injury The intracisternal administration of recombinant rat tumor necrosis factor-α (rrTNF-α) protein in naive rats produced mechanical allodynia and upregulated RIPK1 expression in the TSC. Moreover, an intracisternal pretreatment with Nec-1 inhibited the mechanical allodynia produced by rrTNF-α protein. Nerve injury caused elevated TNF-α concentration in the TSC and a TNF-α block had anti-allodynic effects, thereby attenuating RIPK1 expression in the TSC. Finally, double immunofluorescence analyses revealed the colocalization of TNF receptor and RIPK1 with astrocytes. Hence, we have identified that astroglial RIPK1, activated by the TNF-α pathway, is a central driver of neuropathic pain and that the TNF-α-mediated RIPK1 pathway is a potential therapeutic target for reducing neuropathic pain following nerve injury.

Attenuated febrile response to lipopolysaccharide in rats with biliary obstruction

2000 ◽  
Vol 279 (1) ◽  
pp. G172-G177 ◽  
Author(s):  
L. K. McCullough ◽  
Y. Takahashi ◽  
T. Le ◽  
Q. J. Pittman ◽  
M. G. Swain
Keyword(s):  
Serum Levels ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Febrile Response ◽  
Perioperative Morbidity ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Factor Α ◽  
Generation Male ◽  
Necrosis Factor

Patients with biliary tract obstruction have unexplained, inordinately high rates of perioperative morbidity and mortality, whereas cholestatic animals display abnormal hypothalamic responses to pyrogenic stimuli. We asked if obstructive cholestasis was associated with abnormal fever generation. Male Sprague-Dawley rats (250 g) underwent laparotomy for implantation of thermistors and either bile duct resection (BDR) or sham operation. After recovery, temperatures were recorded by telemetry and conscious, unrestrained rats in each group were injected intraperitoneally with either interleukin-1β (IL-1β;1 μg/kg) or Escherichia colilipopolysaccharide (LPS; 50 μg/kg). Baseline temperatures in both groups were similar. Febrile responses after IL-1β injection in BDR and sham groups were not significantly different. However, in response to LPS injection, BDR rats showed an initial hypothermia with a subsequently attenuated febrile response. Administration of anti-tumor necrosis factor-α (TNF-α) antibody 2 h before LPS injection blocked the LPS-induced hypothermia seen in BDR animals. However, serum levels of TNF-α were not significantly different between sham and BDR animals after LPS injection at any time point measured (0, 1.5, and 3 h).

scholarly journals Antioxidant and Anti-Inflammatory Activities of Biofield Energy Treated Proprietary Test Formulation in Brain Tissues in Cecal Slurry, LPS and E. Coli-Induced Systemic Inflammatory Response Syndrome (SIRS) in Sprague Dawley Rats

2021 ◽  
Vol 1 (3) ◽  
pp. 13-25
Author(s):  
Mahendra Kumar Trivedi ◽  
Alice Branton ◽  
Dahryn Trivedi ◽  
Snehasis Jana
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Systemic Inflammatory Response ◽  
Sprague Dawley ◽  
E Coli ◽  
Test Formulation ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Per Se ◽  
Anti Inflammatory

The study was aimed to evaluate the antioxidant and anti-inflammatory activity of the Biofield Energy Treated Proprietary Test Formulation and Biofield Energy Treatment per se to the animals on Cecal Slurry, LPS and E. coli-induced systemic inflammatory response syndrome (SIRS) model in Sprague Dawley rats. In this experiment, different antioxidants biomarkers such as myeloperoxidase (MPO), superoxide dismutase (SOD), lipid peroxidase (LPO) and cytokines like interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-2 (MIP-2) were analysed using ELISA assay in brain homogenate. A test formulation was formulated including minerals (magnesium, zinc, calcium, selenium, and iron), vitamin C, B6, E, B12, D3, β-carotene, cannabidiol isolate,and Panax ginseng extract. The component of the test formulation were divided into two parts; one section was defined as the untreated, while the other portion of each constituent and three group of animals received Biofield Energy Healing/Blessing Treatment remotely for about 3 minutes by Mr. Mahendra Kumar Trivedi, a renowned spiritual Energy Healer. The level of MPO was significantly (p≤0.001) reduced by 19.43%, 34.91%, 25.43%, 25.29% and 30.33% in the G5 (Cecal Slurry, LPS and E. coli + Biofield Energy Treated test formulation); G6 (Cecal Slurry, LPS and E. coli + Biofield Energy Treatment per se to animals from day -15); G7 (Cecal Slurry, LPS and E. coli + Biofield Energy Treated test formulation from day -15); G8 (Cecal Slurry, LPS and E. coli + Biofield Energy Treatment per se + Biofield Energy Treated/Blessed test formulation from day -15), and G9 (Cecal Slurry, LPS and E. coli + Biofield Energy Treatment per se animals + untreated test formulation) groups, respectively as compared to the untreated test formulation (G4) group. Moreover, the level of SOD was significantly increased by 45.02% (p≤0.001), 16.59%, and 35.99% (p≤0.001) in the G6, G7, and G9 groups, respectively as compared to G4 group. The level of TNF-α was significantly decreased by 12.66%, 46.92% (p≤0.001), 26.57% (p≤0.001), 23.22% (p≤0.001), and 54.28% (p≤0.001) in G5, G6, G7, G8, and G9 groups, correspondingly with reference to G4 group. Moreover, the level of IL-6 was significantly (p≤0.001) decreased by 37.51%, 20.28%, 21.55%, and 33.4% in the G6, G7, G8, and G9 groups, respectively as compared to the G4 group. Additionally, the level of MIP-2 was significantly (p≤0.001) reduced by 47.97%, 17.08%, 20.16% and 26.84% in the G6, G7, G8, and G9 groups, respectively as compared to the G4 group. Together, the data imply the antioxidant and anti-inflammatory potential of the Biofield Energy Treated test formulation and Biofield Energy Treatment per se along with preventive measure on the animal with respect to various inflammatory conditions that might be beneficial various types of systemic inflammatory disorders specially sepsis, trauma, septic shock or any types of injuries. Therefore, the results described a significant reduction of inflammation-related disease progression rate and its complications in the preventive maintenance groups (viz. G6, G7, G8, and G9).

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