scholarly journals Cytokines, Hormones and Cellular Regulatory Mechanisms Favoring Successful Reproduction

2021 ◽  
Vol 12 ◽  
Author(s):  
Marie-Pierre Piccinni ◽  
Raj Raghupathy ◽  
Shigeru Saito ◽  
Julia Szekeres-Bartho
Keyword(s):  
Treg Cells ◽  
Protective Mechanism ◽  
Immune Functions ◽  
Protective Mechanisms ◽  
Th22 Cells ◽  
Beneficial Effects ◽  
Healthy Pregnancy ◽  
Maternal Immune System ◽  
Th17 Cytokine

Its semi-allogeneic nature renders the conceptus vulnerable to attack by the maternal immune system. Several protective mechanisms operate during gestation to correct the harmful effects of anti-fetal immunity and to support a healthy pregnancy outcome. Pregnancy is characterized by gross alterations in endocrine functions. Progesterone is indispensable for pregnancy and humans, and it affects immune functions both directly and via mediators. The progesterone-induced mediator - PIBF - acts in favor of Th2-type immunity, by increasing Th2 type cytokines production. Except for implantation and parturition, pregnancy is characterized by a Th2-dominant cytokine pattern. Progesterone and the orally-administered progestogen dydrogesterone upregulate the production of Th2-type cytokines and suppress the production of Th1 and Th17 cytokine production in vitro. This is particularly relevant to the fact that the Th1-type cytokines TNF-α and IFN-γ and the Th17 cytokine IL-17 have embryotoxic and anti-trophoblast activities. These cytokine-modulating effects and the PIBF-inducing capabilities of dydrogesterone may contribute to the demonstrated beneficial effects of dydrogesterone in recurrent spontaneous miscarriage and threatened miscarriage. IL-17 and IL-22 produced by T helper cells are involved in allograft rejection, and therefore could account for the rejection of paternal HLA-C-expressing trophoblast. Th17 cells (producing IL-17 and IL-22) and Th22 cells (producing IL-22) exhibit plasticity and could produce IL-22 and IL-17 in association with Th2-type cytokines or with Th1-type cytokines. IL-17 and IL-22 producing Th cells are not harmful for the conceptus, if they also produce IL-4. Another important protective mechanism is connected with the expansion and action of regulatory T cells, which play a major role in the induction of tolerance both in pregnant women and in tumour-bearing patients. Clonally-expanded Treg cells increase at the feto-maternal interface and in tumour-infiltrating regions. While in cancer patients, clonally-expanded Treg cells are present in peripheral blood, they are scarce in pregnancy blood, suggesting that fetal antigen-specific tolerance is restricted to the foeto-maternal interface. The significance of Treg cells in maintaining a normal materno-foetal interaction is underlined by the fact that miscarriage is characterized by a decreased number of total effector Treg cells, and the number of clonally-expanded effector Treg cells is markedly reduced in preeclampsia. In this review we present an overview of the above mechanisms, attempt to show how they are connected, how they operate during normal gestation and how their failure might lead to pregnancy pathologies.

scholarly journals Modulation Effects of Curcumin on Erythrocyte Ion-Transporter Activity

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Prabhakar Singh ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Oxidative Stress ◽  
Membrane Lipids ◽  
Curcuma Longa ◽  
Membrane Lipid ◽  
Membrane Transporters ◽  
Protective Mechanism ◽  
Lipid Hydroperoxides ◽  
Beneficial Effects

Curcumin ((1E,6E)-1,7-Bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione), the yellow biphenolic pigment isolated from turmeric (Curcuma longa), has various medicinal benefits through antioxidation, anti-inflammation, cardiovascular protection, immunomodulation, enhancing of the apoptotic process, and antiangiogenic property. We explored the effects of curcuminin vitro(10−5 M to 10−8 M) andin vivo(340 and 170 mg/kg b.w., oral) on Na+/K+ATPase (NKA), Na+/H+exchanger (NHE) activity, and membrane lipid hydroperoxides (ROOH) in control and experimental oxidative stress erythrocytes of Wistar rats. As a result, we found that curcumin potently modulated the membrane transporters activity with protecting membrane lipids against hydro-peroxidation in control as well as oxidatively challenged erythrocytes evidenced by stimulation of NKA, downregulation of NHE, and reduction of ROOH in the membrane. The observed results corroborate membrane transporters activity with susceptibility of erythrocyte membrane towards oxidative damage. Results explain the protective mechanism of curcumin against oxidative stress mediated impairment in ions-transporters activity and health beneficial effects.

scholarly journals Reduction of IL-17A Might Suppress the Th1 Response and Promote the Th2 Response by Boosting the Function of Treg Cells during Silica-Induced Inflammatory ResponseIn Vitro

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Wen Tang ◽  
Fangwei Liu ◽  
Ying Chen ◽  
Laiyu Song ◽  
Wujing Dai ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Diseases ◽  
Treg Cells ◽  
Th2 Response ◽  
Th17 Response ◽  
Th1 Response ◽  
Different Types ◽  
Th17 Cytokine

Silica inhalation can induce chronic lung inflammation and fibrosis. Upon silica stimulation, activated macrophages trigger the T-lymphocyte which can differentiate into many different types of Th cells, including the recently discovered Th17 cells. IL-17A, the typical Th17 cytokine, is reported in some inflammatory diseases. However, the role of IL-17A in silica-induced inflammatory response is still not clear. The regulatory mechanism of silica-induced Th17 response also needs to be investigated. So we established a mice primary cell coculture system (macrophage and lymphocyte) to investigate the role of IL-17A in silica-induced inflammatory responsein vitro, by using anti-IL-17A mAb and IL-1Ra. Both anti-IL-17A mAb and IL-1Ra decreased the level of IL-17A and increased the function of Treg cells. The Th1 response was suppressed and the Th2 response was promoted by the addition of anti-IL-17A mAb or IL-1Ra. IL-1Ra treatment decreased the level of IL-6, whereas the levels of IL-23 and ROR-γt were increased. Our study demonstrated that IL-17A reduction altered the pattern of silica-induced Th responses by boosting the function of Treg cellsin vitro. Blocking the function of IL-1 signal pathway could suppress the level of IL-17A, which played the major role in modulating silica-induced Th responsesin vitro.

Heat shock protein 70 expression protects against sepsis-associated cardiomyopathy by inhibiting autophagy

2020 ◽  
pp. 096032712096575
Author(s):  
Xiaofeng Wang ◽  
Yan Zhu ◽  
Qiuxiang Zhou ◽  
Yueyue Yan ◽  
Jinlong Qu ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Protective Effect ◽  
Heat Shock Protein 70 ◽  
Cecal Ligation ◽  
H9c2 Cell ◽  
Protective Mechanism ◽  
Protective Mechanisms ◽  
Induced Apoptosis

Objectives: Increasing evidence suggests that heat shock protein 70 (Hsp70) has a protective effect in sepsis-induced cardiomyopathy; however, the protective mechanism remains unclear. Methods: Previous studies have also implicated autophagy in sepsis-induced cardiomyopathy. The aim of the current study was to reveal the protective mechanisms of Hsp70 in sepsis-induced cardiomyopathy using a cecal ligation and puncture (CLP) rat sepsis model. The roles of Hsp70 and autophagy in sepsis-induced cardiomyopathy were investigated by pretreating rats with the Hsp70 inhibitor quercetin or the autophagy inhibitor 3-methyladenine (3-Ma) before CLP. We also investigated the protective mechanisms of Hsp70 and the relationship between Hsp70 and autophagy in vitro by stimulating H9c2 cells with lipopolysaccharide (LPS) to simulate sepsis. Results: The result show that inhibition of Hsp70 promoted sepsis-induced death in rats, while inhibition of autophagy inhibited sepsis-induced death. These results suggested that both Hsp70 and autophagy were involved in sepsis-induced cardiomyopathy. Overexpression of Hsp70 in H9c2 myocardial cells in vitro suppressed LPS-induced apoptosis, while inhibition of autophagy with 3-Ma also decreased LPS-induced H9c2 cell apoptosis, suggesting that the protective effect of Hsp70 in sepsis-induced cardiomyopathy was related to autophagy regulation. Conclusion: Overall, these results suggested that Hsp70 protected against sepsis-induced cardiac impairment by attenuating sepsis-induced autophagy.

scholarly journals Edible insects as a source of food bioactives and their potential health effects

2021 ◽  
Vol 14 ◽  
Author(s):  
Klaus Lange ◽  
Yukiko Nakamura
Keyword(s):  
Animal Studies ◽  
Oral Intake ◽  
Edible Insects ◽  
Immune Functions ◽  
Potential Health ◽  
Food Ingredients ◽  
Beneficial Effects

Entomophagy (consumption of insects) is an issue of global nutritional and environmental interest. The nutritional value of insects appears to be high, since they are rich in protein and fat and provide a range of vitamins and minerals. Edible insects contain similar amounts of protein to conventional meat and higher levels of polyunsaturated fatty acids. Due to their high content of protein, micronutrients and fiber, insects could become a valuable alternative to food derived from other animals. The findings of various in vitro and in vivo animal studies suggest beneficial effects of entomophagy with respect to cardiovascular, gastrointestinal and non-communicable diseases as well as immune functions and carcinogenesis. Edible insects appear to be a promising and insufficiently explored source of macronutrients, micronutrients and food bioactives. In the course of time, some edible insects may meet the criteria of functional food ingredients. However, there is a significant lack of research investigating health outcomes in humans. The available evidence in humans, derived from randomized controlled trials, suggests a role of edible insects in the promotion of mineral status and the modulation of gut microbiota, with some prebiotic effects. High-quality clinical studies assessing efficacy, oral intake safety and allergy risk are needed.

scholarly journals Induction of Haemeoxygenase-1 Improves FFA-Induced Endothelial Dysfunction in Rat Aorta

2015 ◽  
Vol 35 (3) ◽  
pp. 1230-1240 ◽  
Author(s):  
Fang Han ◽  
Zongguang Hui ◽  
Shuxian Zhang ◽  
Ningning Hou ◽  
Yali Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
High Sensitivity ◽  
Adenosine Monophosphate ◽  
Rat Aorta ◽  
Superoxide Production ◽  
Protective Mechanism ◽  
No Production ◽  
Beneficial Effects

Background: The induction of haemeoxygenase-1 (HO-1) exerts beneficial effects in the setting of endothelial dysfunction in obesity. High free fatty acid (FFA) levels are a common feature of obesity and are the primary cause of endothelial dysfunction. The objective of our study was to explore the effects of HO-1 induction on FFA-induced endothelial dysfunction in rats. Methods: Rats received FFA treatment with either cobalt protoporphyrin (CoPP) to induce HO-1 or stannous protoporphyrin (SnPP) to inhibit HO-1. Endothelial function was determined by measuring endothelium-dependent vasodilatation (EDV). Nitric oxide (NO) production, superoxide production and nuclear factor (NF)-κB expression in the aorta were each determined. The levels of adenosine monophosphate (AMP)-activated kinase (AMPK) and endothelial nitric oxide synthase (eNOS) expression in endothelial cells were determined via Western blotting. Results: Induction of HO-1 by CoPP decreased circulating FFA, high-sensitivity C-reactive protein and malondialdehyde levels and increased serum adiponectin and glutathione levels compared with the FFA group (P<0.05). High FFA levels resulted in EDV impairment, which was improved by HO-1 induction (P<0.05). Induction of HO-1 increased NO levels and reduced aortic superoxide production and NF-κB expression compared with the FFA group. The FFA group exhibited decreased AMPK expression and eNOS phosphorylation, both of which were enhanced via HO-1 induction (P<0.05). The beneficial effects of CoPP on EDV were partially attenuated in vitro in the presence of inhibitors of AMPK, phosphatidylinositol 3-kinase (PI3K), and eNOS. Conclusions: HO-1 induction with CoPP improves FFA-induced endothelial dysfunction in the rat aorta. The protective mechanism appears to be related to the activation of the AMPK-PI3K-eNOS pathway as a result of increased adiponectin levels as well as decreased inflammation and oxidative stress.

Insight into the mechanism by which metoclopramide improves immune functions after trauma-hemorrhage

2000 ◽  
Vol 279 (1) ◽  
pp. C72-C80 ◽  
Author(s):  
Markus W. Knöferl ◽  
Martin K. Angele ◽  
Alfred Ayala ◽  
William G. Cioffi ◽  
Kirby I. Bland ◽  
...  
Keyword(s):  
Underlying Mechanism ◽  
Sham Operation ◽  
Dependent Manner ◽  
Splenocyte Proliferation ◽  
Immune Functions ◽  
Beneficial Effects ◽  
Plasma Prl ◽  
Tissue Trauma ◽  
Dose Dependent

Although studies have shown that prolactin (Prl) and metoclopramide (Mcp) administration restores the depressed cell-mediated immune functions after hemorrhage, the underlying mechanism responsible for the immunostimulatory effects of Mcp remains unknown. We hypothesized that Mcp improves immune responses by upregulating the secretion of Prl. To test this hypothesis, male C3H/HeN mice were subjected to sham operation or laparotomy (i.e., soft tissue trauma) and hemorrhagic shock (Hem; 35 ± 5 mmHg for 90 min) and then resuscitated. Plasma Prl levels were determined 30 min after Mcp (1 μg/g body wt sc at end of Hem) or vehicle (Veh) treatment in sham and Hem mice. The results indicate that plasma Prl levels increased significantly in Mcp-treated mice (sham-Veh 249.9 ± 5.3, Hem-Veh 229.9 ± 7.6, Hem-Mcp 596.9 ± 73.1 ng/ml, one-way ANOVA, P < 0.05 vs. Veh). To determine whether Mcp produces its salutary effects directly or indirectly via increased Prl secretion, splenocyte proliferation and splenocyte interleukin (IL)-2 and IL-3 release from untreated sham or Hem mice were determined in the presence of increasing concentrations of mouse Prl or Mcp. The addition of Mcp had no effect on splenocyte immune functions in vitro. However, the addition of Prl restored the hemorrhage-induced depressed splenocyte proliferation as well as splenocyte IL-2 and IL-3 release in vitro in a dose-dependent manner. Thus the beneficial effects of Mcp on immune functions after Hem appear to be mediated by Prl. Because Mcp increases plasma levels of the immunoenhancing hormone Prl, this agent should be considered a useful adjunct for the treatment of immunodepression in trauma victims.

scholarly journals Evaluation Of Antioxidant And Cytotoxicity Properties Of Amygdalin Extracted From Prunus Dulcis

2019 ◽  
Vol 6 (2) ◽  
pp. 8-12
Author(s):  
Sushma P ◽  
Bindu Jacob ◽  
Narendhirakannan R.T
Keyword(s):  
Therapeutic Potential ◽  
Tissue Injury ◽  
Scientific Evidence ◽  
Redox Homeostasis ◽  
Antioxidant Property ◽  
Prunus Dulcis ◽  
Antioxidant Defences ◽  
Protective Mechanisms ◽  
Beneficial Effects

Free-radical reactions have been implicated in the pathology of many human diseases like atherosclerosis, ischemic heart disease, aging process, inflammation, diabetes, immuno-suppression,neurodegenerative disease etc. Radicals and other reactive oxygen species are formed constantly in the human body and are removed by the enzymatic and non-enzymatic antioxidant defence. The disturbance in ‘redox homeostasis’ that occurs when antioxidant defences are inadequate can damage lipids, proteins,carbohydrates and DNA. Drugs with multiple protective mechanisms, including antioxidant activity, may be one way of minimizing tissue injury. Phytochemicals with antioxidant property are naturally present in food are of great interest due to their beneficial effects on human health as they offer protection against oxidative deterioration. Amygdalin, also known as vitamin B17 is a cyanogenic glycoside found in several sources mainly in apples, pears, apricots, plums, peaches. Several reports claim amygdalin to be good chemopreventive agent, however these claims are not often backed by proper scientific evidence. Thus the present study is aimed to evaluate the therapeutic potential of amygdalin isolated from Prunus dulcis by studying its in vitro antioxidant and cytotoxic properties.Free-radical reactions have been implicated in the pathology of many human diseases like atherosclerosis, ischemic heart disease, aging process, inflammation, diabetes, immuno-suppression,neurodegenerative disease etc. Radicals and other reactive oxygen species are formed constantly in the human body and are removed by the enzymatic and non-enzymatic antioxidant defence. The disturbance in ‘redox homeostasis’ that occurs when antioxidant defences are inadequate can damage lipids, proteins,carbohydrates and DNA. Drugs with multiple protective mechanisms, including antioxidant activity, may be one way of minimizing tissue injury. Phytochemicals with antioxidant property are naturally present in food are of great interest due to their beneficial effects on human health as they offer protection against oxidative deterioration. Amygdalin, also known as vitamin B17 is a cyanogenic glycoside found in several sources mainly in apples, pears, apricots, plums, peaches. Several reports claim amygdalin to be good chemopreventive agent, however these claims are not often backed by proper scientific evidence. Thus the present study is aimed to evaluate the therapeutic potential of amygdalin isolated from Prunus dulcis by studying its in vitro antioxidant and cytotoxic properties.

Phenolic Acids Exert Anticholinesterase and Cognition-Improving Effects

2018 ◽  
Vol 15 (6) ◽  
pp. 531-543 ◽  
Author(s):  
Dominik Szwajgier ◽  
Ewa Baranowska-Wojcik ◽  
Kamila Borowiec
Keyword(s):  
Phenolic Acids ◽  
Ex Vivo ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
Amyloid Β Peptide ◽  
Beneficial Effects ◽  
Aβ Fibrils

Numerous authors have provided evidence regarding the beneficial effects of phenolic acids and their derivatives against Alzheimer's disease (AD). In this review, the role of phenolic acids as inhibitors of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) is discussed, including the structure-activity relationship. In addition, the inhibitory effect of phenolic acids on the formation of amyloid β-peptide (Aβ) fibrils is presented. We also cover the in vitro, ex vivo, and in vivo studies concerning the prevention and treatment of the cognitive enhancement.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia?

2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis
Keyword(s):  
Heart Failure ◽  
Insulin Treatment ◽  
Close Association ◽  
Adverse Outcomes ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Treatment Of Diabetes

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

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