scholarly journals Qiu’s Neiyi Recipe Regulates the Inflammatory Action of Adenomyosis in Mice via the MAPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Pian Ying ◽  
Hui Li ◽  
Yan Jiang ◽  
Zhitao Yao ◽  
Shenyi Lu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mapk Signaling ◽  
The Body ◽  
Erk Signaling ◽  
Inflammatory Factors ◽  
Control Group ◽  
Histological Changes ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Promising Treatment

Background. The management of adenomyosis is challenging and limiting. Qiu’s Neiyi recipe (Qiu) is a traditional Chinese medicine (TCM) prescription clinically used for endometriosis treatment in China, but the effect and mechanism of Qiu on adenomyosis are undefined. Methods. An experimental adenomyosis model was induced in female neonatal ICR mice administrated with tamoxifen. The adenomyosis mice were divided into five groups: high-, middle-, and low-Qiu’s group, danazol group, and model group. The mice just administrated with the solvent only (no tamoxifen or drugs) were served as the control group. After 28 days of administration, the body, uterine, spleen, and thymus weights of all mice were examined. Then, the myometrial infiltration and the expression of inflammatory factors were detected by histology examination, ELISA, and qRT-PCR in the uterus. In addition, the MAPK/ERK signaling pathway-related protein expression in adenomyosis mice was detected by immunohistochemical (IHC) staining, qRT-PCR, and western blotting. Results. In experimental adenomyosis mice, Qiu treatment improved the symptoms of adenomyosis by reducing the myometrial infiltration and increasing the index of spleen and thymus. The elevated levels of IL-1β, IL-6, and TNF-α in serum and uterus tissues of adenomyosis model mice were also decreased after Qiu treatment. The improvement of Qiu on the adenomyosis was achieved by inhibiting the activated MAPK/ERK signaling pathway, including reducing the mRNA and protein expressions of p-ERK/ERK, p-JNK/JNK, and p-p38/p38 in the uterus tissues. Conclusion. Qiu alleviated the inflammatory reaction and uterus histological changes in mice with adenomyosis, and the potential mechanism is through the inhibition of the MAPK/ERK signaling pathway. Qiu may be a promising treatment for adenomyosis.

scholarly journals DAP Inhibits the TNF-α-Induced Inflammatory Response by Modulating the MAPK Signaling Pathway in Synovial Cells

2021 ◽  
Author(s):  
Jieying Wang ◽  
Nanzhen Kuang ◽  
Mao zheng ◽  
Chan Dai ◽  
Huimin Deng ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Inflammatory Factors ◽  
Control Group ◽  
Synovial Cells ◽  
Tnf Α ◽  
Model Control

Abstract Daphnetin(DAP) is extracted from Daphne odora var. marginata and contains coumarin compounds, which have a good anti-inflammatory analgesic effect. In this study, we investigated whether daphnetin can reduce the TNF-α-induced inflammatory response by inhibiting the MAPK signaling pathway in the synovial cells of CIA rats. A model of synovial cells was constructed using CIA rats induced by TNF-α. The expression of inflammatory cytokines in the synovial cells of CIA rats was observed by real-time PCR and ELISA. The expression and nuclear translocation of MAPK signaling pathway proteins were detected by Western blot and immunofluorescence assays. The results show that the mRNA and protein levels of IL-6, TGF-β, MMP-3 and MMP-13 were significantly lower than those in the culture supernatant of the model control group. The synovial cells of CIA rats induced by TNF-α exhibited decreased expression of p-p38, p-ERK1/2 and p-JNK in the nucleus. In conclusion, daphnetin can affect the activation of the MAPK signaling pathway and reduce the expression of inflammatory factors by inhibiting the MAPK signaling pathway, which plays a role in anti-rheumatic inflammation.

scholarly journals NOD-like receptors mediate inflammatory lung injury during plateau hypoxia exposure

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Haiyan Wang ◽  
Xue Lin ◽  
Xiaoyan Pu
Keyword(s):  
Lung Injury ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Enrichment Analysis ◽  
Mapk Signaling ◽  
The Body ◽  
Inflammatory Factors ◽  
Hypoxia Exposure ◽  
Tnf Α ◽  
Mapk Signaling Pathways

Abstract Background The lung is an important target organ for hypoxia treatment, and hypoxia can induce several diseases in the body. Methods We performed transcriptome sequencing for the lungs of rats exposed to plateau hypoxia at 0 day and 28 days. Sequencing libraries were constructed, and enrichment analysis of the differentially expressed genes (DEGs) was implemented using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Subsequently, experimental validation was executed by quantitative real-time PCR (qRT-PCR) and western blot. Results The results showed that the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) signaling pathway that was involved in immunity may play a crucial function in lung injury caused by plateau hypoxia. And the expressions of NOD1, NOD2, IL-1β, TNF-α, IL-6, and IL-18 were higher at 28 days of exposure to plateau hypoxia than that at 0 day. Similarly, CARD9, MYD88, p38 MAPK, and NF-κB p65, which are related to the NF-κB and MAPK signaling pathways, also demonstrated increased expression at 28 days exposure to plateau hypoxia than at 0 day. Conclusions Our study suggested that the NF­κBp65 and p38 MAPK signaling pathways may be activated in the lungs of rats during plateau hypoxia. Upregulated expression of NF­κBp65 and p38 MAPK can promote the transcription of downstream inflammatory factors, thereby aggravating the occurrence and development of lung tissue remodeling.

scholarly journals Tetrahydropalmatinee alleviates diabetic neuropathic pain by inhibiting the inflammation via p38-MAPK signaling pathway in microglia

2021 ◽  
Author(s):  
Lianzhi Cheng ◽  
Junlong Ma ◽  
Aijuan Jiang ◽  
Kai Cheng ◽  
Fanjing Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Inflammatory Factors ◽  
Specific Marker ◽  
Diabetic Neuropathic Pain ◽  
Tnf Α

Abstract Object: Exploring the effect of Tetrahydropalmatine (THP) on diabetic neuropathic pain (DNP) and its possible mechanism. Methods: The type 2 diabetic (T2DM) rat models were prepared by high-fat and high-sugar feeding combined with a single small-dose intraperitoneal injection of streptozotocin (STZ). When the mechanical withdrawal threshold (MWT) and the thermal withdrawal latency (TWL) of T2DM model rats decreased to less than 85% which were judged as DNP-bearing rats. After treatment with or without THP, the protein expression of hypertonic glycerol reactive kinase (p38), phosphorylated hypertonic glycerol-responsive kinase (p-p38) and OX42 (a specific marker of microglia) were detected by Western Blot and and the mRNA content of p38 and OX42 were detected by qRT-PCR. The expression of pro-inflammatory factors IL-1β, IL-6, TNF-α, as well as chemotactic factors and their receptors including CXCL1, CXCR2, CCL2 and CCR2 in spinal tissues were detected by ELISA. Serum FINS and GSP content were also detected by ELISA. Double-label immunofluorescence were used to observe the expression of OX42 and p-p38 in the spinal dorsal horn. Results: Results showed that THP inhibited microglial activation of spinal in DNP rats. And after THP intervention, the MWT and TWL of DNP rats decreased, the expression of p38, p-p38 and OX42 in the spinal cord tissues of rats was significantly reduced while the mRNA of p38 and OX42 also reduced. The expression of IL-1β, IL-6, TNF-α, CXCL1, CXCR2, CCL2 and CCR2 in the spinal cord tissues of rats was significantly reduced (P < 0.01). At the same time, THP significantly proved FINS, but did not affect FBG and GSP in DNP rats. Conclusions: THP significantly alleviates pain symptoms in DNP rats, and this effect may be achieved by inhibiting the inflammatory response caused by the activation of microglia mediated by the p38-MAPK signaling pathway.

scholarly journals Role of ESAT-6 in renal injury by regulating microRNA-155 expression via TLR4/MyD88 signaling pathway in mice with Mycobacterium tuberculosis infection

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Zhong-Qi Zhou ◽  
Zhi-Kui Wang ◽  
Lei Zhang ◽  
Yue-Qin Ren ◽  
Zhong-Wei Ma ◽  
...  
Keyword(s):  
Body Weight ◽  
Mycobacterium Tuberculosis ◽  
Signaling Pathway ◽  
Renal Injury ◽  
Control Group ◽  
Interleukin 17 ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Ifn Γ ◽  
Myd88 Signaling

The study aims to investigate the underlying mechanism involved in the early secretory antigenic target-6 (ESAT-6) in renal injury through regulation of the expression of miR-155 through the oll-like receptor (TLR)-4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway in Mycobacterium tuberculosis (MTB)-infected mice. Sixty C57BL/6 mice with MTB-induced renal injury were randomly assigned into control, MTB, mimic, inhibitor, inhibitor + ESAT6, and inhibitor + ESAT6 + TAK242 groups. Body weight, the ratio of kidney weight to body weight (Kw/Bw), blood urea nitrogen (BUN), and serum creatinine (Scr) of mice were measured. Flow cytometry was used to detect renal activation in mice. Expressions of miR-155 and ESAT6 were detected by quantitative real-time PCR (qRT-PCR), and Western blotting was used to examine the expressions of ESAT6, TLR4, and MyD88. Expressions of tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), and interferon-γ (IFN-γ) were measured by qRT-PCR and ELISA. Compared with the control group, the BUN and Scr levels as well as the expression levels of miR-155, TLR4, MyD88, TNF-α, IL-17, and IFN-γ increased, while Kw/Bw decreased in the MTB and mimic groups. In comparison with the MTB group, the above indexes except Kw/Bw were elevated in the mimic group, but were reduced in the inhibitor group, while the Kw/Bw dropped in the mimic group but increased in the inhibitor group. Compared with the inhibitor group, the Kw/Bw decreased while the rest of the indexes increased in the inhibitor + ESAT6 group. ESAT6 may induce renal injury by promoting miR-155 expression through the TLR-4/MyD88 signaling pathway in MTB-infected mice.

scholarly journals Disorders of Major Inflammatory Factors and Histopathological Lesions in Excess-iron-fed Sheep Liver

2021 ◽  
Author(s):  
LiangYu Zhang ◽  
Jing Lu ◽  
FengJiao Sun ◽  
XiaoPing Lv ◽  
ChaoNan Liu ◽  
...  
Keyword(s):  
Disease Diagnosis ◽  
The Body ◽  
Inflammatory Factors ◽  
Control Group ◽  
Excess Iron ◽  
Sheep Liver ◽  
Histopathological Lesions ◽  
Tnf Α ◽  
Ifn Γ ◽  
Tgf Β1

Abstract Background: Iron plays a key role in biological metabolism as an essential microelement. Excess iron may cause pathological damage to the body. The purpose of this work is to explore the disorders of major inflammatory factors and histopathological lesions in the liver of excess-iron-fed sheep. Twenty German Mutton Merino sheep were randomly divided into 4 groups, control group (CON), iron-excess group one (IronE1), iron-excess group two (IronE2) and iron-excess group three (IronE3), respectively. Each group was fed with basal diets supplemented with 50 (CON), 500 (IronE1), 1000 (IronE2), and 1500 (IronE3) mg/kg as ferrous sulfate monohydrate (FeSO4 ·H2O). After 75 days, the liver was removed and collected. A variety of methods were utilized to detect indicators of sheep liver. Results: The histopathological damage of liver in sheep was rather severe with the excess of iron. Hemosiderin deposits were also obviously discovered. The results also showed that the expression of both protein and mRNA of IL-1β, TNF-α and IFN-γ reduced, but the factors of IL-2, IL-6, NF-κB and TGF-β1 obviously increased in the liver of each iron excess group. Corresponding changes were also discovered with the addition of iron dosage. The content of inflammatory factors above showed a significant change with an addition of 1500 mg/kg iron into the basic diet, which indicated that excess iron inhibited the release of IL-1β, TNF-α and IFN-γ in the sheep liver. The inflammation caused by excess iron extenuated by reducing the content of these three pro-inflammatory factors. The expression of IL-2, IL-6, NF-κB and TGF-β1 increased. As pro-inflammatory factors induced inflammation, anti-inflammatory factors also increased to protect the body from tissue damage. Conclusions: It can be concluded that excess iron can change the expression of main inflammatory factors in sheep liver, which will be an instructive significance to the development of medical prospect for sheep breeding and disease diagnosis.

Effects of Moringa Oleifera Leaf Polysaccharide on Growth Performance and Immune Response of Broiler Chickens

2021 ◽  
Author(s):  
Hosameldeen Mohamed Husien ◽  
JunJie Huang ◽  
WeiLong Peng ◽  
ShuMei Zheng ◽  
JinGui Li
Keyword(s):  
Immune Response ◽  
Growth Performance ◽  
Broiler Chickens ◽  
Moringa Oleifera ◽  
The Body ◽  
Feed Consumption ◽  
Feed Additive ◽  
Control Group ◽  
High Dose ◽  
Tnf Α

Abstract Moringa oleifera (MO) is a widely used as the nutritious and non-traditional feed supplementation containing kinds of bioactive substances. However, the enhancement effect of Moringa oleifera leaf Polysaccharide (MOLP) as a feed additive in broilers growth performance and immunity remains unclear. In this study, MOLP was obtained by water extraction and alcohol precipitation method, then purified with Trichloroacetic acid (TCA) assay. Chickens were randomly divided into 4 groups, to receive different doses of MOLP (0, 0.1, 0.2, 0.4g/kg) in feed for 3 weeks. The body weight gain (BWG) and feed consumption were recorded for feed conversion ratio (FCR) and average daily feed intake (ADFI) calculation. Broiler chickens were sacrificed and sampled on day 14, 21, 28 (D 14, D 21, and D 28) respectively. Serological indicators, including total protein (TP), albumin (ALB), globulin (GLO), and creatinine (CREA) were detected. ELISA kits were applied for detecting the levels of immunoglobulin A (IgA), immunoglobulin G (IgG), interleukin-2 (IL-2), and tumor necrosis factor (TNF-α). From D 21 to D 28, the results showed that middle dose of MOLP significantly increased BWG and ADFI as well as liver and bursa indexes when compared with the control group. In addition, TP and GLO were also increased (P<0.05). All MOLP treatments enhanced the serum concentrations of IgG and IL-2 (P<0.01). Furthermore, results of quantitative RT-PCR showed that high dose of MOLP treatment significantly increased (P<0.001) the mRNA expression levels of IL-2 and TNF-α of chickens relative to the control group. In conclusion, the results showed that MOLP supplementation contributed to improve growth performance and immune response in broiler chickens, and MOLP could be considered as a promising feed additive.

Role of testosterone in regulating induction of TNF-α in rat spleen via ERK signaling pathway

Steroids ◽  
2016 ◽  
Vol 111 ◽  
pp. 148-154 ◽  
Author(s):  
Chien-Wei Chen ◽  
Cai-Yun Jian ◽  
Po-Han Lin ◽  
Chih-Chieh Chen ◽  
Fu-Kong Lieu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Erk Signaling ◽  
Tnf Α

scholarly journals EFFECT OF ZINC ELEMENT AND DEXAMETHASONE ON SOME HEMATOLOGICAL BIOCHEMICAL TESTS IN RABBITS MALE

2016 ◽  
Vol 47 (6) ◽  
Author(s):  
D. S. Dheyab
Keyword(s):  
Blood Cells ◽  
White Blood Cells ◽  
The Body ◽  
Control Group ◽  
Blood Collection ◽  
Biochemical Tests ◽  
Histological Changes ◽  
Spleen Tissue ◽  
Cholesterol Levels ◽  
Short Time

This study was conducted to investigate the effect of zinc in dose 15mg/kg.bw daily  taken by the mouth and dexamethasone 4mgIkg.Bw by injection for 30days on some hematological biochemical tests and some histological changes of liver spleen in male rabbits. Thirty rabbits were used that divided into 3 randomized groups (each group contain 10 male rabbits ). Control group was taken normal food and water, Zinc group that gave zinc at dose of 15mg/kg.BW/daily/oral on 1, 2, 3, 4 weeks. Dexamethasone with zinc group : Employ dexamethasone 4mg/Kg.Bw . I.M dialy for 1 and 2 weeks for experiment and at  3, 4th weeks they gave zn 15mg/lKg.Bw day/orally. Blood samples were taken from the heart directly in 2 and 4weeks to examine packed cell volume (pcv), white blood cells (WBCs), Red blood cells (RBCs) with differential Leuckcyte count.separation blood collection to plasma and examine glucose mg/dl , cholesterol mg/dl. In histological tests, rabbits were killed and separate their organs tissue from the body to examine liver and spleen. The results revealed  a decrease in level of RBCs, pcv after treatment with zinc 15, mg/Kg.Bw orally (zinc group) and increase in WBCs with differential leuckocyte count specially neutrophil cell, while biochemical tests show increase in glucose and cholesterol levels after treatment with dexamethasone 4mglkgBw. I/M seen increase in counts of RBCs , PCV, WBCs and differential lenkocyte count and decrease in glucose with cholesterol parameters, histological changes show change in liver after treatment by dexamethasone 4mglKg.Bw ,spleen tissue seen necrosis and pigmentation with hemorrhage after take dexamethasone 4mglkg in (dexamethasone + zinc group). Results also showed that zinc enhanced the immune system in at normal dose for limited time  because of its effect on other mineral such as copper and causes anemia , while the dexamethasone is a drug used for antianflammatory but for a short time.                                                                                                                           

scholarly journals Effects of Shugan-Jianpi Recipe on the Expression of the p38 MAPK/NF-κB Signaling Pathway in the Hepatocytes of NAFLD Rats

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 106 ◽  
Author(s):  
Yuanjun Deng ◽  
Kairui Tang ◽  
Runsen Chen ◽  
Yajie Liu ◽  
Huan Nie ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Low Dose ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Dose ◽  
Model Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: In traditional Chinese medicine, the Shugan-Jianpi recipe is often used in the treatment of nonalcoholic fatty liver disease (NAFLD). This study aimed to explore the mechanism of the Shugan-Jianpi recipe in relation to rats with NAFLD induced by a high-fat diet. Methods: Rats were randomly divided into eight groups: normal group (NG), model group (MG), low-dose Chaihu–Shugan–San group (L-CG), high-dose Chaihu–Shugan–San group (H-CG), low-dose Shenling–Baizhu–San group (L-SG), high-dose Shenling–Baizhu–San group (H-SG), low dose of integrated-recipes group (L-IG), and high dose of integrated-recipes group (H-IG). After 26 weeks, a lipid profile, aspartate, and alanine aminotransferases in serum were detected. The serum levels of inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed using the enzyme linked immunosorbent assay (ELISA) method. Hepatic pathological changes were observed with hematoxylin-eosin (HE) and oil red O staining. The expression of the p38 mitogen-activated protein kinases (MAPK)/nuclear factor-κB (NF-κB) pathway was detected by quantitative real-time PCR and Western blotting. Results: A pathological section revealed that NAFLD rats have been successfully reproduced. Compared with the model group, each treatment group had different degrees of improvement. The Shugan-Jianpi recipe can inhibit the serum levels of IL-1β, IL-6, and TNF-α in NAFLD rats. The expression of mRNA and a protein related to the p38 MAPK/NF-κB signaling pathway were markedly decreased as a result of the Shugan-Jianpi recipe. Conclusions: The Shugan-Jianpi recipe could attenuate NAFLD progression, and its mechanism may be related to the suppression of the p38 MAPK/NF-κB signaling pathway in hepatocytes.

scholarly journals Preoperative pain aggravates postoperative cognitive deficits and hippocampal neuroinflammation in rats

2019 ◽  
Author(s):  
Xiang Gao ◽  
Xian Ding ◽  
Huan Yi ◽  
Chuan-tao Lin ◽  
Yu-ping Wang ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Inflammatory Factors ◽  
Control Group ◽  
Gamma Aminobutyric Acid ◽  
Sprague Dawley ◽  
Preoperative Pain ◽  
Pain Model ◽  
Simple Operation ◽  
Tnf Α ◽  
Operation Group

Abstract Background Perioperative neurocognitive disorder (PND) is the progressive deterioration of cognitive function after surgery. The purpose of this study was to observe the effect of preoperative pain on inflammatory factors and neuronal apoptosis in the hippocampus of rats. Methods 36 adult male Sprague-Dawley rats were randomly divided into 4 groups: the control group, the pain group, the pain+operation group, and the operation group. 6 days before the surgery, the rats received cognitive training, and the cognitive evaluation was carried out on the1, 3 and 7th days after the surgery. The rats were killed on the first, third and seventh days after the surgery (n = 3 rats/day). The cognitive function of rats was evaluated by the Morris Water Maze (MWM), and the expression levels of the pro-inflammatory cytokines interleukin 6(IL-6), Interleukin 1β(IL-1β)and Tumor Necrosis Factor-α(TNF-α), Acetylcholine(Ach)and Cyclic Adenosine monophosphate(cAMP), protein kinase A(PKA)and gamma-aminobutyric acid type A receptors(GABAA) in the hippocampus were measured on the 1st, 3rd and 7th days after the operation. Results Our results showed that the pain model rats exhibited impaired behavior on the first day (P< 0.001), and this lasted until the 7th day after the operation (P≤0.002 and P≤0. 001, respectively). Preoperative pain model rats showed a higher level of apoptosis than that shown by the simple operation rats. On the 1st, 3rd and 7th days after the operation, the protein content of IL-1β, IL-6 and TNF-α in the pain operation group was increased compared to that in the simple operation group (P<0.001). ACh, cAMP, PKA and GABAA expression in the hippocampus was decreased after operation in the preoperative pain model rats. Conclusion Preoperative pain is a key risk factor for the development of PND. The ACh-PKA-GABAA signaling pathway plays a key role in the acetylcholine pathway.

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