scholarly journals Ursodeoxycholic Acid Exhibits Anti-inflammatory Activity against Concanavalin A-induced Immune Hepatitis in Mice

2021 ◽  
Author(s):  
Guixian Ji ◽  
Man Liu ◽  
Yi Zhou ◽  
Weilong Zhong ◽  
Xiaoyi Wang ◽  
...  
Keyword(s):  
Ursodeoxycholic Acid ◽  
Concanavalin A ◽  
Suppressor Cells ◽  
Inflammatory Factors ◽  
Inflammatory Factor ◽  
Interacting Protein ◽  
Hepatic Macrophages ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α

Abstract ObjectiveIt was to evaluate the anti-inflammatory effect of ursodeoxycholic acid (UDCA) on concanavalin A (ConA)-induced immune hepatitis in mice and determine the molecular mechanism. MethodsFemale C57BL/6J mice were randomly classified into Control, ConA, and ConA+UDCA groups. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of hepatic inflammatory factor tumor necrosis factor-α (TNF-α), and receptor-interacting protein (RIP)3 mRNA. The percentages of immune cells in liver and spleen were detected and analyzed by flow cytometry. ResultsUDCA decreased the serum ALT and AST levels, down-regulated the expression of cytokine TNF-α mRNA and necroptosis marker RIP3 mRNA in the liver tissue, up-regulated the percentages of immunomodulatory myeloid-derived suppressor cells (MDSCs) in liver and spleen tissues, and down-regulated the accumulation of liver macrophages of mice with immune hepatitis. ConclusionsUDCA attenuates ConA-induced hepatic inflammation in mice by reducing the production of hepatic inflammatory factors, inhibiting the expression of necroptosis signal proteins in hepatocytes, down-regulating the accumulation of hepatic macrophages, and increasing the percentage of MDSCs with immunomodulatory properties.

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.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

scholarly journals Biomimetic nanotherapy: core–shell structured nanocomplexes based on the neutrophil membrane for targeted therapy of lymphoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qiangqiang Zhao ◽  
Duanfeng Jiang ◽  
Xiaoying Sun ◽  
Qiuyu Mo ◽  
Shaobin Chen ◽  
...  
Keyword(s):  
Mesoporous Silica Nanoparticles ◽  
Treatment Options ◽  
Inflammatory Factors ◽  
Main Method ◽  
Tnf Α ◽  
Good Biocompatibility ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
New Treatment ◽  
Lymphoma Therapy

Abstract Background Non-Hodgkin’s lymphoma (NHL) is a malignant disease of lymphoid tissue. At present, chemotherapy is still the main method for the treatment of NHL. R-CHOP can significantly improve the survival rate of patients. Unfortunately, DOX is the main cytotoxic drug in R-CHOP and it can lead to adverse reactions. Therefore, it is particularly important to uncover new treatment options for NHL. Results In this study, a novel anti-tumor nanoparticle complex Nm@MSNs-DOX/SM was designed and constructed in this study. Mesoporous silica nanoparticles (MSNs) loaded with Doxorubicin (DOX) and anti-inflammatory drugs Shanzhiside methylester (SM) were used as the core of nanoparticles. Neutrophil membrane (Nm) can be coated with multiple nanonuclei as a shell. DOX combined with SM can enhance the anti-tumor effect, and induce apoptosis of lymphoma cells and inhibit the expression of inflammatory factors related to tumorigenesis depending on the regulation of Bcl-2 family-mediated mitochondrial pathways, such as TNF-α and IL-1β. Consequently, the tumor microenvironment (TME) was reshaped, and the anti-tumor effect of DOX was amplified. Besides, Nm has good biocompatibility and can enhance the EPR effect of Nm@MSNs-DOX/SM and increase the effect of active targeting tumors. Conclusions This suggests that the Nm-modified drug delivery system Nm@MSNs-DOX/SM is a promising targeted chemotherapy and anti-inflammatory therapy nanocomplex, and may be employed as a specific and efficient anti-Lymphoma therapy.

scholarly journals From Inflammation to the Onset of Fibrosis through A2A Receptors in Kidneys from Deceased Donors

2020 ◽  
Vol 21 (22) ◽  
pp. 8826
Author(s):  
Elena Guillén-Gómez ◽  
Irene Silva ◽  
Núria Serra ◽  
Francisco Caballero ◽  
Jesús Leal ◽  
...  
Keyword(s):  
Deceased Donor ◽  
Inflammatory Factors ◽  
Mrna Levels ◽  
A2a Adenosine Receptor ◽  
A2a Receptors ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Pka Pathway ◽  
Tgf Β1 ◽  
M2 Phenotype

Pretransplant graft inflammation could be involved in the worse prognosis of deceased donor (DD) kidney transplants. A2A adenosine receptor (A2AR) can stimulate anti-inflammatory M2 macrophages, leading to fibrosis if injury and inflammation persist. Pre-implantation biopsies of kidney donors (47 DD and 21 living donors (LD)) were used to analyze expression levels and activated intracellular pathways related to inflammatory and pro-fibrotic processes. A2AR expression and PKA pathway were enhanced in DD kidneys. A2AR gene expression correlated with TGF-β1 and other profibrotic markers, as well as CD163, C/EBPβ, and Col1A1, which are highly expressed in DD kidneys. TNF-α mRNA levels correlated with profibrotic and anti-inflammatory factors such as TGF-β1 and A2AR. Experiments with THP-1 cells point to the involvement of the TNF-α/NF-κB pathway in the up-regulation of A2AR, which induces the M2 phenotype increasing CD163 and TGF-β1 expression. In DD kidneys, the TNF-α/NF-κB pathway could be involved in the increase of A2AR expression, which would activate the PKA–CREB axis, inducing the macrophage M2 phenotype, TGF-β1 production, and ultimately, fibrosis. Thus, in inflamed DD kidneys, an increase in A2AR expression is associated with the onset of fibrosis, which may contribute to graft dysfunction and prognostic differences between DD and LD transplants.

scholarly journals Anti-Allergic and Anti-Inflammatory Effects of Undecane on Mast Cells and Keratinocytes

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1554
Author(s):  
Dabin Choi ◽  
Wesuk Kang ◽  
Taesun Park
Keyword(s):  
Mast Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Allergic Diseases ◽  
Intracellular Camp ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Skin Conditions ◽  
Factor Α ◽  
Camp Levels

The critical roles of keratinocytes and resident mast cells in skin allergy and inflammation have been highlighted in many studies. Cyclic adenosine monophosphate (cAMP), the intracellular second messenger, has also recently emerged as a target molecule in the immune reaction underlying inflammatory skin conditions. Here, we investigated whether undecane, a naturally occurring plant compound, has anti-allergic and anti-inflammatory activities on sensitized rat basophilic leukemia (RBL-2H3) mast cells and HaCaT keratinocytes and we further explored the potential involvement of the cAMP as a molecular target for undecane. We confirmed that undecane increased intracellular cAMP levels in mast cells and keratinocytes. In sensitized mast cells, undecane inhibited degranulation and the secretion of histamine and tumor necrosis factor α (TNF-α). In addition, in sensitized keratinocytes, undecane reversed the increased levels of p38 phosphorylation, nuclear factor kappaB (NF-κB) transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). These results suggest that undecane may be useful for the prevention or treatment of skin inflammatory disorders, such as atopic dermatitis, and other allergic diseases.

AGGF1 is a novel anti-inflammatory factor associated with TNF-α-induced endothelial activation

2013 ◽  
Vol 25 (8) ◽  
pp. 1645-1653 ◽  
Author(s):  
Fang-Yuan Hu ◽  
Chong Wu ◽  
Yang Li ◽  
Ke Xu ◽  
Wen-Jing Wang ◽  
...  
Keyword(s):  
Endothelial Activation ◽  
Inflammatory Factor ◽  
Tnf Α ◽  
Anti Inflammatory

scholarly journals Anti-inflammatory reflex action of splanchnic sympathetic nerves is distributed across abdominal organs

2019 ◽  
Vol 316 (3) ◽  
pp. R235-R242 ◽  
Author(s):  
Davide Martelli ◽  
David G. S. Farmer ◽  
Michael J. McKinley ◽  
Song T. Yao ◽  
Robin M. McAllen
Keyword(s):  
Sympathetic Nerves ◽  
Target Organ ◽  
Inflammatory Pathway ◽  
Splanchnic Nerves ◽  
Abdominal Organs ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
The Difference ◽  
Factor Α ◽  
Inflammatory Action

The splanchnic anti-inflammatory pathway has been proposed as the efferent arm of the inflammatory reflex. Although much evidence points to the spleen as the principal target organ where sympathetic nerves inhibit immune function, a systematic study to locate the target organ(s) of the splanchnic anti-inflammatory pathway has not yet been made. In anesthetized rats made endotoxemic with lipopolysaccharide (LPS, 60 µg/kg iv), plasma levels of tumor necrosis factor-α (TNF-α) were measured in animals with cut (SplancX) or sham-cut (Sham) splanchnic nerves. We confirm here that disengagement of the splanchnic anti-inflammatory pathway in SplancX rats (17.01 ± 0.95 ng/ml, mean ± SE) strongly enhances LPS-induced plasma TNF-α levels compared with Sham rats (3.76 ± 0.95 ng/ml). In paired experiments, the responses of SplancX and Sham animals were compared after the single or combined removal of organs innervated by the splanchnic nerves. Removal of target organ(s) where the splanchnic nerves inhibit systemic inflammation should abolish any difference in LPS-induced plasma TNF-α levels between Sham and SplancX rats. Any secondary effects of extirpating organs should apply to both groups. Surprisingly, removal of the spleen and/or the adrenal glands did not prevent the reflex splanchnic anti-inflammatory action nor did the following removals: spleen + adrenals + intestine; spleen + intestine + stomach and pancreas; or spleen + intestine + stomach and pancreas + liver. Only when spleen, adrenals, intestine, stomach, pancreas, and liver were all removed did the difference between SplancX and Sham animals disappear. We conclude that the reflex anti-inflammatory action of the splanchnic nerves is distributed widely across abdominal organs.

scholarly journals Macrophage Populations and Expression of Regulatory Inflammatory Factors in Hepatic Macrophage-depleted Rat Livers under Lipopolysaccharide (LPS) Treatment

2018 ◽  
Vol 46 (5) ◽  
pp. 540-552 ◽  
Author(s):  
Munmun Pervin ◽  
Mohammad Rabiul Karim ◽  
Mizuki Kuramochi ◽  
Takeshi Izawa ◽  
Mitsuru Kuwamura ◽  
...  
Keyword(s):  
Low Dose ◽  
Inflammatory Factors ◽  
M2 Macrophage ◽  
Related Factors ◽  
Macrophage Activity ◽  
Hepatic Macrophages ◽  
Tnf Α ◽  
Macrophage Populations ◽  
Rat Livers ◽  
Lps Treatment

To investigate the significance of the appearance of hepatic macrophages and expression of inflammatory factors in normal and macrophage-depleted livers, hepatic macrophages were depleted with liposome (Lipo)-encapsulated clodronate (CLD; 50 mg/kg, i.v.) followed by lipopolysaccharide (LPS) administration (0.1 mg/kg, i.p.) in F344 rats (CLD + LPS). Vehicle control rats (Lipo + LPS) received empty-Lipo before LPS. The low dose of LPS did not result in microscopic changes in the liver in either treatment group but did modulate M1 and M2 macrophage activity in Lipo + LPS rats without altering repopulating hepatic macrophages in CLD + LPS rats. LPS treatment in Lipo + LPS rats dramatically increased the M1 (IL-1β, IL-6, TNF-α, and MCP-1) but not M2 macrophage-related factors (IL-4 and CSF-1) compared to CLD + LPS rats. In the CLD + LPS rats, the M2 macrophage-related factors IL-4 and CSF-1 were elevated. In conclusion, low-dose LPS activated hepatic macrophages in rat livers without causing liver injury or stimulating repopulating hepatic macrophages. These data suggest that LPS may alter the liver microenvironment by modulating M1 or M2 macrophage-related inflammatory mediators and macrophage-based hepatotoxicity.

Ulinastatin Activated The ERK5/Mer Signaling Pathway To Promote Macrophage Efferocytosis And Ameliorate Lung Inflammation

2021 ◽  
Author(s):  
Jinju Li ◽  
Rongge Shao ◽  
Qiuwen Xie ◽  
XueKe Du
Keyword(s):  
Lung Injury ◽  
Signaling Pathway ◽  
Lung Inflammation ◽  
Raw264.7 Cells ◽  
Inflammatory Factors ◽  
Inflammatory Factor ◽  
Dependent Manner ◽  
Anti Inflammatory

Abstract Purpose:Ulinastatin (UTI) is an endogenous protease inhibitor with potent anti-inflammatory, antioxidant and organ protective effects. The inhibitor has been reported to ameliorate inflammatory lung injury but precise mechanisms remain unclear. Methods: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). The number of neutrophils and the phagocytosis of apoptotic neutrophils were observed by Diff- Quick method. Lung injury was observed by HE staining .BALF cells were counted by hemocytometer and concentrations of protein plus inflammatory factors were measured with a BCA test kit. During in vitro experiments, RAW264.7 cells were pretreated with UTI (1000 and 5000U/ mL), stained with CellTrackerTM Green B0DIPYTM and HL60 cells added with UV-induced apoptosis and PKH26 Red staining. The expression of ERK5\Mer related proteins was detected by western blot and immunofluorescence.Results: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). UTI treatment enhanced the phagocytotic effect of mouse alveolar macrophages on neutrophils, alleviated lung lesions, decreased the pro-inflammatory factor and total protein content of BALF and increased levels of anti-inflammatory factors. in vitro experiments ，UTI enhanced the phagocytosis of apoptotic bodies by RAW264.7 cells in a dose-dependent manner. Increased expression levels of ERK5 and Mer by UTI were shown by Western blotting and immunofluorescence.Conclusions: UTI mediated the activation of the ERK5/Mer signaling pathway, enhanced phagocytosis of neutrophils by macrophages and improved lung inflammation. The current study indicates potential new clinical approaches for accelerating the recovery from lung inflammation.

scholarly journals Essential Oil of Myrtus communis Inhibits Inflammation in Rats by Reducing Serum IL-6 and TNF-α

2011 ◽  
Vol 6 (10) ◽  
pp. 1934578X1100601 ◽  
Author(s):  
Andrea Maxia ◽  
Maria Assunta Frau ◽  
Danilo Falconieri ◽  
Manvendra Singh Karchuli ◽  
Sanjay Kasture
Keyword(s):  
Essential Oil ◽  
Inflammatory Activity ◽  
Myrtus Communis ◽  
Ear Edema ◽  
Tnf Α ◽  
Cotton Pellet ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

The topical anti-inflammatory activity of the essential oil of Myrtus communis L. was studied using croton oil induced ear edema and myeloperoxidase (MPO) activity in mice, and cotton pellet induced granuloma, and serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in rats. On topical application, the oil exhibited a significant decrease in the ear edema as well as MPO activity. The oil also inhibited cotton pellet-induced granuloma and serum TNF-α and IL-6. It can be concluded that the essential oil of Myrtus communis reduces leukocyte migration to the damaged tissue and exhibits anti-inflammatory activity.

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