scholarly journals Experimental Study of the Effect of Serum Hydrogen Sulfide on the Course of the Inflammatory Process in the Vaginal Wall

Author(s):  
Dmytro Grebeniuk ◽  
Natalia Voloshchuk ◽  
Oleksandr Nazarchuk ◽  
Nataliia Dzis ◽  
Illia Taran ◽  
...  

Introduction: Various pathological conditions are characterized by the influence of hydrogen sulfide level on the course of the pathological process. This study examines the effect of serum hydrogen sulfide levels on the inflammatory process in the vaginal wall of rats. Aims: To evaluate the effect of excess and deficiency of serum hydrogen sulfide on the course of the inflammatory process in the vaginal wall of rats. Methodology: The study was performed on 125 female Wistar rats under 1 year of age and weighing 160.0 to 200.0 grams. All animals were divided into 7 groups: control (intact rats) and 6 experimental groups with different H2S levels and different treatment approaches of inflammation in the vaginal wall. The level of serum hydrogen sulfide was studied and the levels of TNF-α and IL-1β in the tissue homogenate of the vaginal wall were determined. In all experimental groups, the study was performed in dynamics - 10 min, 4, 8 and 24h after simulation of inflammation. Results: The dynamics of local levels of TNF-α and IL-1β in all groups had a similar trend and was characterized by the rapid development of the inflammatory process from its simulation to 4 hours of study, followed by gradual attenuation of inflammation and almost complete normalization of the studied indicators for 24 hours. Preliminary serial introduction of sodium hydrosulfide, as a donor of hydrogen sulfide, allowed to reduce the degree of manifestation of the inflammatory process and to achieve faster normalization of the studied parameters. At the same time, the artificially created deficiency of serum hydrogen sulfide (previous serial administration of propargylglycine) prolonged the duration and increased the studied indicators of inflammation in the vaginal wall. Conclusions: The course and intensity of the inflammatory process in the vaginal wall of rats are directly dependent on the background level of serum hydrogen sulfide.

Author(s):  
D. I. Grebeniuk ◽  
N. I. Voloshchuk ◽  
I. V. Taran ◽  
P. P. Gormash ◽  
O. A. Nazarchuk

Various pathological conditions can be characterized not only by a decrease or increase in basal levels of hydrogen sulfide in the serum, but also the levels of hydrogen sulfide can modulate the course of the pathological process. The impact of serum hydrogen sulfide on the condition of the intact vaginal wall of rats was evaluated in this study. The aim of the study was to evaluate the effect of excess and deficiency of serum hydrogen sulfide on the condition of the vaginal wall of intact rats. The study was performed on 75 female Wistar rats under 1 year of age and weighing 160.0 to 200.0 grams. All animals were divided into 6 groups: control (intact rats); experimental 1 (H2S excess); experimental 2 (H2S deficiency); experimental 3 (intravaginal administration of suppositories with clindamycin); experimental 4 (H2S excess + suppositories with clindamycin); experimental 5 (H2S deficiency + suppositories with clindamycin). The levels of serum hydrogen sulfide were studied, as well as microscopic examination of the structure of the vaginal wall and determination of the levels of TNF-α and IL-1β in tissue homogenate were performed. In experimental groups 3, 4 and 5 all studies were performed in dynamics – 10 minutes, 4, 8 and 24 hours after a single intravaginal administration of clindamycin phosphate. The data were processed using the statistical software package SPSS 20.0 for Windows. Under conditions of both hydrogen sulfide deficiency and excess, no statistically significant changes in TNF-α and IL-1β levels in the vaginal wall of intact rats were observed. Also, no changes in the histological structure of the wall were found. Similar data were demonstrated in experimental groups 3, 4 and 5. This picture is explained by the fact that hydrogen sulfide affects various parts of the inflammatory process, while reducing the production of inflammatory mediators. In intact tissues, in the absence of an inflammatory process, there is no point of application of hydrogen sulfide, and therefore no significant changes are observed. Thus, both excess and deficiency of serum hydrogen sulfide do not affect the condition of the vaginal wall of intact rats.


2015 ◽  
Vol 309 (11) ◽  
pp. E925-E935 ◽  
Author(s):  
Li Sun ◽  
Song Zhang ◽  
Chengyuan Yu ◽  
Zhenwei Pan ◽  
Yang Liu ◽  
...  

Autophagy plays an important role in liver triglyceride (TG) metabolism. Inhibition of autophagy could reduce the clearance of TG in the liver. Hydrogen sulfide (H2S) is a potent stimulator of autophagic flux. Recent studies showed H2S is protective against hypertriglyceridemia (HTG) and noalcoholic fatty liver disease (NAFLD), while the mechanism remains to be explored. Here, we tested the hypothesis that H2S reduces serum TG level and ameliorates NAFLD by stimulating liver autophagic flux by the AMPK-mTOR pathway. The level of serum H2S in patients with HTG was lower than that of control subjects. Sodium hydrosulfide (NaHS, H2S donor) markedly reduced serum TG levels of male C57BL/6 mice fed a high-fat diet (HFD), which was abolished by coadministration of chloroquine (CQ), an inhibitor of autophagic flux. In HFD mice, administration of NaSH increased the LC3BII-to-LC3BI ratio and decreased the p62 protein level. Meanwhile, NaSH increased the phosphorylation of AMPK and thus reduced the phosphorylation of mTOR in a Western blot study. In cultured LO2 cells, high-fat treatment reduced the ratio of LC3BII to LC3BI and the phosphorylation of AMPK, which were reversed by the coadministration of NaSH. Knockdown of AMPK by siRNA in LO2 cells blocked the autophagic enhancing effects of NaSH. The same qualitative effect was observed in AMPKα2−/− mice. These results for the first time demonstrated that H2S could reduce serum TG level and ameliorate NAFLD by activating liver autophagy via the AMPK-mTOR pathway.


2015 ◽  
Vol 75 (3) ◽  
Author(s):  
T. Zaga ◽  
D. Makris ◽  
I. Tsilioni ◽  
T. Kiropoulos ◽  
S. Oikonomidi ◽  
...  

Background and Aim. Hyaluronic acid (HA) is a component of extracellular matrix and may play a role in the pleural inflammation which is implicated in parapneumonic effusions.The aim of the current study was to investigate HA levels in serum and pleura in patients with parapneumonic effusions. Methods. We prospectively studied pleural and serum levels of HA in 58 patients with pleural effusions due to infection (complicated and uncomplicated parapneumonic effusions), malignant effusions and transudative effusions due to congestive heart failure. In addition to HA, TNF-α and IL-1β levels were determined in pleural fluid and serum by ELISA. Results. The median±SD HA levels (pg/ml) in pleural fluid of patients with complicated effusions (39.058±11.208) were significantly increased (p<0.005), compared to those with uncomplicated parapneumonic effusions (11.230±1.969), malignant effusions (10.837±4.803) or congestive heart failure (5.392±3.133). There was no correlation between pleural fluid and serum HA values. Pleural fluid TNF-α levels (146±127 pg/mL) and IL-1β levels (133.4±156 pg/mL) were significantly higher in patients with complicated parapneumonic effusions compared to patients with other types of effusion (p<0.05). No significant association between HA and TNF-α or IL-1β was found. Conclusions. HA may play a significant role in the inflammatory process which characterises exudative infectious pleuritis. Further investigation might reveal whether HA is a useful marker in the management of parapneumonic effusions.


Author(s):  
Adryan Fristiohady ◽  
Muhammad Hajrul Malaka ◽  
Andi Rizqa Wahyuni Safitri ◽  
Dewo Diha ◽  
Saripuddin Saripuddin ◽  
...  

Inflammation is the host's protective response to any stimulus that harms the body. Excessive inflammatory process causes tissue damage. Therefore, an anti-inflammatory agent is needed. The use of natural ingredients, especially sea sponges, is an option to reduce the side effects of anti-inflammatory agents. This utilization is related to the discovery of new agents. So, we tested the effect of the ethanol extract of Petrosia sp. as an anti-inflammatory agent. Animal induced with 1% carrageenan and left for 1 hour. After that the animals were divided into 6 groups (n = 4) and given oral treatment, namely: Group I (normal group); Group II (negative group); Group III (ethanol extract of Petrosia sp. Concentration of 0.05mg/ml); Group IV (ethanol extract of Petrosia sp. Concentration 0.1mg/ml); Group V (ethanol extract of Petrosia sp. Concentration 0.2mg/ml); and Group VI (positive group, Diclofenac Sodium). After 1 hour, the animals were measured for edema volume and plasma TNF-α levels. Based on the research conducted, the ethanol extract of Petrosia sp. decreased edema volume and plasma TNF-α levels in inflammatory mice. The concentration of 0.2mg/mL had a significant effect on the negative control used (p <0.05). On the other hand, Petrosia sp. indicates the presence of alkaloids, flavonoids, and steroids. They may play an important role in the anti-inflammatory process. Thus, it can be concluded that the ethanol extract of Petrosia sp. has anti-inflammatory activity.


2020 ◽  
Vol 73 (11) ◽  
pp. 2427-2430
Author(s):  
Sergii V. Shevchuk ◽  
Yuliia S. Seheda ◽  
Inna P. Kuvikova ◽  
Olena V. Shevchuk ◽  
Olena Y. Galiutina

The aim: Was to evaluate the effect of 6-month pathogenetic treatment in combination with atorvastatinum on the endothelium function, lipid and adipokine levels, paroxonase activity and activity of inflammatory process in RA patients. Materials and methods: The study included 55 patients with RA, dividing into two groups depending on the intended therapy. The first group included 33 patients with “traditional” treatment by methotrexate, glucocorticoids, and non-steroid anti-inflammatory drugs. The second group included 22 patients with “traditional” treatment and additionally prescribed of atorvastatinum 20 mg/day. The lipid profile, leptin, adipokine, paroxonase activity. C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) levels, FMDBA and IMT of carotid artery were determined in all participants of the study. Control parameters were recorded before the start, after 1 and 6 months of treatment. Results: The FMDBA has increased by 32% in the second group, compared by only 10.9% in the first group. The dynamics of IMT in the first group was also twice lower than in group with the additional use of atorvastatinum. The leptin levels in the second group significantly decreased by 27% and adiponectin levels increased by 12.8%, than in the first group – by 12.8% and by 7% respectively. The appointment of statins over 6 months resulted in DAS28, TNF-α, ESR and CRP reduction by 15%, 31%, 25% and 21.5% respectively. In the first group the dynamics of indicate rates ranged from 7.8% to 22.5%, and was significantly lower than in the second group. Conclusions: As a result of the study, it was found that the appointment of atorvastatinum 20 mg/day during 6 months not only reduces dyslipidemia, but also significantly reduces the inflammatory process and adipokine dysregulation, normalizes serum paraoxonase activity and improves the endothelium function.


Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1682 ◽  
Author(s):  
Michaela Kosutova ◽  
Olga Pechanova ◽  
Andrej Barta ◽  
Sona Franova ◽  
Martina Cebova

Myocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two groups of 16-week-old WKY rats. In one group, NO production was inhibited by L-NAME (20 mg/kg/day) administration four weeks prior to ligation. Sham operations were performed on both groups as a control. Seven days after MI, we evaluated levels of nitric oxide synthase (NOS) activity, eNOS, iNOS, NFҡB/p65 and Nrf2 in ischemic, injured and non-ischemic zones of the heart. Levels of circulating TNF-α and IL-6 were evaluated in the plasma. MI led to increased NOS activity in all investigated zones of myocardium as well as circulating levels of TNF-α and IL-6. L-NAME treatment decreased NOS activity in the heart of sham operated animals. eNOS expression was increased in the injured zone and this could be a compensatory mechanism that improves the perfusion of the myocardium and cardiac dysfunction. Conversely, iNOS expression increased in the infarcted zone and may contribute to the inflammatory process and irreversible necrotic changes.


Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 603
Author(s):  
Cengiz Kaya ◽  
Bernardo Murillo-Amador ◽  
Muhammad Ashraf

The aim of this study is to assess the role of l-cysteine desulfhydrase (l-DES) and endogenous hydrogen sulfide (H2S) in glutathione (GSH)-induced tolerance to salinity stress (SS) in sweet pepper (Capsicum annuum L.). Two weeks after germination, before initiating SS, half of the pepper seedlings were retained for 12 h in a liquid solution containing H2S scavenger, hypotaurine (HT), or the l-DES inhibitor dl-propargylglycine (PAG). The seedlings were then exposed for three weeks to control or SS (100 mmol L−1 NaCl) and supplemented with or without GSH or GSH+NaHS (sodium hydrosulfide, H2S donor). Salinity suppressed dry biomass, leaf water potential, chlorophyll contents, maximum quantum efficiency, ascorbate, and the activities of dehydroascorbate reductase, monodehydroascorbate reductase, and glyoxalase II in plants. Contrarily, it enhanced the accumulation of hydrogen peroxide, malondialdehyde, methylglyoxal, electrolyte leakage, proline, GSH, the activities of glutathione reductase, peroxidase, catalase, superoxide dismutase, ascorbate peroxidase, glyoxalase I, and l-DES, as well as endogenous H2S content. Salinity enhanced leaf Na+ but reduced K+; however, the reverse was true with GSH application. Overall, the treatments, GSH and GSH+NaHS, effectively reversed the oxidative stress and upregulated salt tolerance in pepper plants by controlling the activities of the AsA-GSH and glyoxalase-system-related enzymes as well as the levels of osmolytes.


2020 ◽  
Vol 11 ◽  
Author(s):  
Longna Li ◽  
Yuhao Liu ◽  
Shu Wang ◽  
Jianxin Zou ◽  
Wenjiang Ding ◽  
...  

Magnesium hydride (MgH2) is a promising solid-state hydrogen source with high storage capacity (7.6 wt%). Although it is recently established that MgH2 has potential applications in medicine because it sustainably supplies hydrogen gas (H2), the biological functions of MgH2 in plants have not been observed yet. Also, the slow reaction kinetics restricts its practical applications. In this report, MgH2 (98% purity; 0.5–25 μm size) was firstly used as a hydrogen generation source for postharvest preservation of flowers. Compared with the direct hydrolysis of MgH2 in water, the efficiency of hydrogen production from MgH2 hydrolysis could be greatly improved when the citrate buffer solution is introduced. These results were further confirmed in the flower vase experiment by showing higher efficiency in increasing the production and the residence time of H2 in solution, compared with hydrogen-rich water. Mimicking the response of hydrogen-rich water and sodium hydrosulfide (a hydrogen sulfide donor), subsequent experiments discovered that MgH2-citrate buffer solution not only stimulated hydrogen sulfide (H2S) synthesis but also significantly prolonged the vase life of cut carnation flowers. Meanwhile, redox homeostasis was reestablished, and the increased transcripts of representative senescence-associated genes, including DcbGal and DcGST1, were partly abolished. By contrast, the discussed responses were obviously blocked by the inhibition of endogenous H2S with hypotaurine, an H2S scavenger. These results clearly revealed that MgH2-supplying H2 could prolong the vase life of cut carnation flowers via H2S signaling, and our results, therefore, open a new window for the possible application of hydrogen-releasing materials in agriculture.


2019 ◽  
Vol 97 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Kürşad Aytekin ◽  
Selma Şengiz Erhan ◽  
Züleyha Erişgin ◽  
Cem Zeki Esenyel ◽  
Selçuk Takır

Hydrogen sulfide (H2S) is found in both the plasma and synovial fluid of patients with gonarthrosis. In the present study, we investigated whether intra-articular injection of sodium hydrosulfide (NaSH) (1 mM, 30 μL), a H2S donor, might affect gonarthrosis in rats. Gonarthrosis was induced surgically in the left knees of rats and left for 6 weeks for the development of disease. Then, intra-articular injections of NaSH or methylprednisolone (1 mg/kg, 30 μL) were administered to rats. Half of each group was sacrificed at the end of the first day and the other half was sacrificed at the end of 4 weeks to evaluate early and later effects of injections on gonarthrosis. The injury induced by anterior cruciate ligament resection and medial meniscectomy in rats caused the development of gonarthrosis. As the duration lengthened after gonarthrosis induction, the progression of the disease continued. According to the modified Mankin Scoring System, intra-articular injection of NaSH histopathologically slowed the progression of gonarthrosis, whereas methylprednisolone was ineffective. In addition, NaSH decreased apoptosis in rat knees with gonarthrosis. Each treatment did not cause injury to healthy knees. Our results lead to the consideration that intra-articular NaSH administration may be effective in the progression of gonarthrosis.


2016 ◽  
Vol 310 (1) ◽  
pp. H71-H79 ◽  
Author(s):  
Maggie M. Kuo ◽  
Dae Hee Kim ◽  
Sandeep Jandu ◽  
Yehudit Bergman ◽  
Siqi Tan ◽  
...  

Hydrogen sulfide (H2S) has emerged as an important gasotransmitter in the vasculature. In this study, we tested the hypothesis that H2S contributes to coronary vasoregulation and evaluated the physiological relevance of two sources of H2S, namely, cystathionine-γ-lyase (CSE) and 3-mercaptypyruvate sulfertransferase (MPST). MPST was detected in human coronary artery endothelial cells as well as rat and mouse coronary artery; CSE was not detected in the coronary vasculature. Rat coronary artery homogenates produced H2S through the MPST pathway but not the CSE pathway in vitro. In vivo coronary vasorelaxation response was similar in CSE knockout mice, wild-type mice (WT), and WT mice treated with the CSE inhibitor propargylglycine, suggesting that CSE-produced H2S does not have a significant role in coronary vasoregulation in vivo. Ex vivo, the MPST substrate 3-mercaptopyruvate (3-MP) and H2S donor sodium hydrosulfide (NaHS) elicited similar coronary vasoreactivity responses. Pyruvate did not have any effects on vasoreactivity. The vasoactive effect of H2S appeared to be nitric oxide (NO) dependent: H2S induced coronary vasoconstriction in the presence of NO and vasorelaxation in its absence. Maximal endothelial-dependent relaxation was intact after 3-MP and NaHS induced an increase in preconstriction tone, suggesting that endothelial NO synthase activity was not significantly inhibited. In vitro, H2S reacted with NO, which may, in part explain the vasoconstrictive effects of 3-MP and NaHS. Taken together, these data show that MPST rather than CSE generates H2S in coronary artery, mediating its effects through direct modulation of NO. This has important implications for H2S-based therapy in healthy and diseased coronary arteries.


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