scholarly journals Varicocele-Mediated Male Infertility: From the Perspective of Testicular Immunity and Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Yiwei Fang ◽  
Yufang Su ◽  
Jia Xu ◽  
Zhiyong Hu ◽  
Kai Zhao ◽  
...  
Keyword(s):  
Testicular Tissue ◽  
Normal Function ◽  
Inflammatory Factors ◽  
Immune Microenvironment ◽  
Inflammatory Pathways ◽  
Pyrin Domain ◽  
Abnormal Increase ◽  
Precision System ◽  
Sperm Antibodies ◽  
Necrosis Factor

BackgroundVaricocele (VC) is present in 35 - 40% of men with infertility. However, current surgical and antioxidant treatments are not completely effective. In addition to oxidative stress, it is likely that other factors such as testicular immune microenvironment disorder contribute to irreversible testicular. Evidence suggests that VC is associated with anti-sperm antibodies (ASAs), spermatogenesis and testosterone secretion abnormalities, and testicular cytokine production. Moreover, inhibition of inflammation can alleviate VC-mediated pathogenesis. The normal function of the testis depends on its immune tolerance mechanism. Testicular immune regulation is complex, and many infectious or non-infectious diseases may damage this precision system.ResultsThe testicular immune microenvironment is composed of common immune cells and other cells involved in testicular immunity. The former includes testicular macrophages, T cells, dendritic cells (DCs), and mast cells, whereas the latter include Leydig cells and Sertoli cells (SCs). In animal models and in patients with VC, most studies have revealed an abnormal increase in the levels of ASAs and pro-inflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha in the seminal plasma, testicular tissue, and even peripheral blood. It is also involved in the activation of potential inflammatory pathways, such as the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing (NLRP)-3 pathway. Finally, the development of VC-mediated infertility (VMI) may be facilitated by abnormal permeability of proteins, such as claudin-11, that constitute the blood-testis barrier (BTB).ConclusionsThe testicular immune response, including the production of ASAs and inflammatory factors, activation of inflammatory pathways, and destruction of the BTB may be involved in the pathogenesis of VMI it is necessary to further explore how patient outcomes can be improved through immunotherapy.

scholarly journals Inflammasome Signaling and Other Factors Implicated in Atherosclerosis Development and Progression

2020 ◽  
Vol 26 (22) ◽  
pp. 2583-2590 ◽  
Author(s):  
Zeinab Nazarian-Samani ◽  
Robert D. E. Sewell ◽  
Mahmoud Rafieian-Kopaei
Keyword(s):  
Type 2 Diabetes ◽  
Arterial Occlusion ◽  
Inflammatory Factors ◽  
Inflammatory Pathways ◽  
Pyrin Domain ◽  
Inflammatory Mechanism ◽  
Life Threatening ◽  
Domain 3 ◽  
Atherosclerosis Development

Chronic inflammation plays an extensive role in the onset and progression of metabolic disorders such as atherosclerosis, type 2 diabetes, gout and obesity. Atherosclerosis accounts for up to 70% mortality in patients with type 2 diabetes and is also a chronic condition that causes atrial stenosis due to a lipometabolism imbalance. The purpose of this article is to consider the inflammatory factors implicated in atherosclerosis and their role in the development and progression of this vascular disease. The inflammasome signaling pathway is an important inflammatory mechanism involved in the development of atherosclerosis. The most important inflammasome pathway in this respect is the NLRP3 inflammasome (Nucleotide-binding oligomerization domain (NOD)-like receptor with a pyrin domain 3), whose activation leads to the generation of important inflammatory cytokines including interleukins 1β and 18 (IL-1β and 18). The activities of these mature cytokines and inflammatory factors produced by other inflammatory pathways lead to arterial inflammation and eventually arterial occlusion, which can result in life-threatening complications such as myocardial infarction and stroke. Therefore, it is essential to seek out more precise mechanisms for the activation of inflammasomes and other inflammatory pathways for the development of therapeutic strategies of atherosclerosis.

scholarly journals Dexmedetomidine Inhibits Nlrp3 Inflammasome Priming in BV-2 microglia through the NF-κB Pathway and the ROS-Nlrp3-IL-1β Signaling Axis

2021 ◽  
Author(s):  
Jiawei Xie ◽  
Li Chen ◽  
Yuling Luo ◽  
Jianling Li ◽  
Xianxue Wang ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Inflammatory Factors ◽  
Pyrrolidine Dithiocarbamate ◽  
Neurocognitive Dysfunction ◽  
Pyrin Domain ◽  
Tnf Α ◽  
Signaling Axis ◽  
The Impact ◽  
Necrosis Factor ◽  
Receptor Family

Abstract In the brain, the NOD-like receptor family pyrin domain containing 3 (Nlrp3) inflammasome is mostly expressed in microglia and is considered to be the primary cause of perioperative neurocognitive dysfunction (PND). Dexmedetomidine (Dex), a novel kind of clinical anesthetic with anti-inflammatory properties, has been shown to be effective in preventing PND in surgical patients. However, the mechanism of its anti-neuroinflammatory activity is still quite unclear. We examined the impact of Dex administration on Nlrp3 priming in activated BV-2 cells in this research. To investigate the mechanism by which Dex impacts Nlrp3 priming, we employed the inhibitors pyrrolidine dithiocarbamate (PDTC) and N-acetyl-L-cysteine (NAC) to block the NF-κB p65 and the reactive oxygen species (ROS)-Nlrp3-interleukin (IL)-1β signaling axis, respectively. The results showed that Dex substantially decreased the expression of Nlrp3 and p65 and significantly inhibited the levels of the inflammatory factors IL-1β and tumor necrosis factor (TNF)-α in BV-2 cells stimulated with lipopolysaccharide (LPS). Additionally, when the NF-κB pathway was inhibited by PDTC, Dex could aggravate the downregulation of Nlrp3 and IL-1β in BV-2 cells. What is more, Dex negatively regulated the expression of Nlrp3 and IL-1β in activated BV-2 cells when NAC was added. These results showed that Dex inhibited Nlrp3 priming in LPS-induced BV-2 cells, presumably via blocking the NF-κB pathway and the ROS-Nlrp3-IL-1β signaling axis.

scholarly journals Lipopolysaccharides promote pulmonary fibrosis in silicosis through the aggravation of apoptosis and inflammation in alveolar macrophages

2020 ◽  
Vol 15 (1) ◽  
pp. 598-605
Author(s):  
Shiyi Tan ◽  
Shang Yang ◽  
Mingke Chen ◽  
Yurun Wang ◽  
Li Zhu ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Alveolar Macrophages ◽  
Inflammatory Factors ◽  
Necrosis Factor Alpha ◽  
Defensive Role ◽  
Factor Alpha ◽  
Apoptosis And Inflammation ◽  
The Relationship ◽  
Lps Treatment ◽  
Necrosis Factor

AbstractAlveolar macrophages (AMs) play an important defensive role by removing dust and bacteria from alveoli. Apoptosis of AMs is associated with lung fibrosis; however, the relationship between this apoptotic event and environmental factors, such as the presence of lipopolysaccharides (LPSs) in the workplace, has not yet been addressed. To investigate whether exposure to LPS can exacerbate fibrosis, we collected AMs from 12 male workers exposed to silica and incubated them in the presence and absence of LPS for 24 h. We show that the levels of cleaved caspase-3 and pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha were increased in these AMs following LPS treatment. Moreover, we demonstrate that LPS exposure aggravated apoptosis and the release of inflammatory factors in AMs in a mouse model of silicosis, which eventually promoted pulmonary fibrosis. These results suggest that exposure to LPS may accelerate the progression of pulmonary fibrosis in silicosis by increasing apoptosis and inflammation in AMs.

scholarly journals Astaxanthin protective barrier and its ability to improve the health in patients with COVID-19

2021 ◽  
Author(s):  
Ali-Reza Ahmadi ◽  
Roya Ayazi-Nasrabadi
Keyword(s):  
Distress Syndrome ◽  
Novel Species ◽  
Good Health ◽  
Inflammatory Factors ◽  
Necrosis Factor Alpha ◽  
Inflammatory Agent ◽  
Tnf Α ◽  
Factor Alpha ◽  
Cox 2 ◽  
Necrosis Factor

Inflammation acts like a double-edged sword and can be harmful if not appropriately controlled. COVID-19 is created through a novel species of coronavirus SARS-CoV-2 (2019-nCoV). Elevated levels of inflammatory factors such as inter- leukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), etc. lead to Acute Respiratory Distress Syndrome (ARDS) and severe complications of infection in the lungs of coronavirus-infected patients. Astaxanthin is a natural and potent carotenoid with powerful antioxidant activity as well as an anti-inflammatory agent that supports good health. The effects of astaxanthin on the regulation of cyclooxygenase-2 (COX-2) pathways and the reduction and suppression of cytokines and other inflam- matory agents such as IL-6 and TNF-α have already been identified. Therefore, these unique features can make this natural compound an excellent option to minimize inflammation and its consequences.

Mammalian Target of Rapamycin (mTOR) Inhibitor Improves Local Immune Microenvironment and Reduces Seizures via Increasing miR-211 Level in Rat Brain

2022 ◽  
Vol 12 (4) ◽  
pp. 841-847
Author(s):  
Meijiao Du ◽  
Zhengmei Wang ◽  
Geng Su ◽  
Yunxia Zhou ◽  
Chuan Luo
Keyword(s):  
Rat Brain ◽  
Brain Tissue ◽  
Mtor Inhibitor ◽  
Symptom Relief ◽  
Mtor Inhibitors ◽  
Inflammatory Factors ◽  
Control Group ◽  
Tunel Staining ◽  
Immune Microenvironment ◽  
Rat Brain Tissue

This study aims to analyze the role of mTOR inhibitor on the expression of miR-211 in rat brain tissue and the biological effect of miR-211 in attenuating seizure. Rats were randomly divided into four groups, and the number of seizures and the duration of single seizure were observed within 24 hours after intervention. The level of miR-211 in brain tissue was detected by RT qPCR, the apoptosis of nerve cells was assessed by TUNEL staining, the level of immune cells was detected by flow cytometry, and the level of serum inflammatory factors was determined by ELISA. The number of seizures and the duration of single seizure in the three groups treated by rapamycin within 24 hours were lower than those in the control group, and the symptom relief in group C was the best. After treatment, the expression level of miR-211 in the brain tissue of epileptic rats increased. TUNEL staining showed that neuronal apoptosis was obvious in epileptic rats. The anti apoptotic ability of group C was the most significant, followed by group D and group B. Compared with group A, the levels of CD3+ cells, CD8+ cells and CD4+/CD25+ cells in brain tissue of group C were decreased, while the levels of IL-2 and IFN-γ were lower in group C than those in control. In group C (n = 5), the levels of CD3+ cells, CD8+ cells and CD4+/CD25+ cells were elevated, and the levels of immune related cytokines IL-2 and IFN-γ were higher than those of rats without miR-211 inhibition. mTOR inhibitors can improve the local immune microenvironment, reduce the release of inflammatory factors, and finally decrease the frequency and duration of seizures by up regulating the level of miR-211 in rat brain tissue.

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.

Pterostilbene Ameliorates Nephropathy Injury in Streptozotocin-Induced Diabetic Rats

Pharmacology ◽  
2019 ◽  
Vol 104 (1-2) ◽  
pp. 71-80 ◽  
Author(s):  
Ying Zhang ◽  
Shaoyu Ren ◽  
Ying Ji ◽  
Yafeng Liang
Keyword(s):  
High Fat Diet ◽  
Nuclear Factor Κb ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Necrosis Factor ◽  
Different Doses

Background: Our study investigated the therapeutic role and potential mechanisms of pterostilbene (PS) in diabetic nephropathy (DN) rats. Methods: DN models were established by high-fat diet after streptozotocin injection. A total of 50 Sprague-Dawley rats were randomly divided into control, DN, PS-treated groups (PS-H, PS-M, PS-L). PS was administered to rats by gavage for 8 weeks at 3 different doses (25, 10, and 5 mg/kg/day). The levels of oxidative stress activity (superoxide dismutase [SOD], malondialdehyde [MDA], glutathione peroxidase [GSH-PX]) and inflammatory factors (tumor necrosis factor [TNF]-α, interleukin (IL)-6, IL-1β, monocyte chemoattractant factor [MCP]-1) were detected by ­ELISA. TGF-β, Smad1, and fibronectin (FN) were measured through immunohistochemistry. The relative expressions of phospho-IκBα/IκBα, phospho-IκB kinases (IKK)β/IKKβ, phospho-nuclear factor-κB (NF-κB) p65/NF-κB p65 were detected by western blot. Results: Compared with DN group, the levels of TNF-α, IL-6, IL-1β, and MCP-1 were decreased in the PS-H group (p < 0.05). Meanwhile, the levels of SOD, MDA, GSH-PX improved in kidney and serum in PS-H groups (p< 0.05). PS also significantly decreased the level of phospho-NF-κB p65 and increased the levels of phospho- IKKβ and phospho-Iκ-Bα (p < 0.05). The results showed that PS treatment decreased TGF-β, Smad1, and FN expressions. Conclusion: PS had potential therapeutic effects on DN, which may be related to the regulation of NF-κB pathway.

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.

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