scholarly journals A study on the protective effects of CpG ODN-induced mucosal immunity against lung injury in a mouse ARDS model

2018 ◽  
Author(s):  
Guan Wang ◽  
Zong-Jian Liu ◽  
Xuan Liu ◽  
Feng-Ge Liu ◽  
Yan Li ◽  
...  
Keyword(s):  
Intranasal Administration ◽  
Distress Syndrome ◽  
Tissue Injury ◽  
Rectal Administration ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Cpg Odn ◽  
Animal Investigation ◽  
Unmethylated Cytosine ◽  
Severe Lung

AbstractThis study aims to determine the feasibility of using oligodeoxynucleotides with unmethylated cytosine-guanine dinucleotide sequences (CpG ODN) as an immunity protection strategy for a mouse model of acute respiratory distress syndrome (ARDS). This is a prospective laboratory animal investigation. 20-week old BALB/c mice in Animal research laboratory were randomized into groups. An ARDS model was induced in mice using lipopolysaccharides. CpG ODN was intranasally and transrectally immunized before or after the 3rd and 7th day of establishing the ARDS model. Mice were euthanized on day seven after the 2nd immunization. Then, retroorbital bleeding was carried, out and the chest was rapidly opened to collect the trachea and tissues from both lungs for testing. CpG ODN significantly improved the pathologic impairment in mice lung, especially after the intranasal administration of 50 ug. This resulted in the least severe lung tissue injury. Furthermore, IL-6 and IL-8 concentrations were lower, which was second to mice treated with the rectal administration of 20 μg CpG ODN. In contrast, the nasal and rectal administration of CpG ODN in BALB/c mice before LPS immunization did not appear to exhibit any significant protective effects. In conclusion, the intranasal administration of CpG ODN may be is a potential treatment approach to ARDS. More studies are needed to further determine the protective mechanism of CpG ODN.

scholarly journals Therapeutic Potential of Heme Oxygenase-1/Carbon Monoxide in Lung Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Myrna Constantin ◽  
Alexander J. S. Choi ◽  
Suzanne M. Cloonan ◽  
Stefan W. Ryter
Keyword(s):  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Therapeutic Potential ◽  
Tissue Injury ◽  
Heme Oxygenase 1 ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Oxidative Breakdown ◽  
Biliverdin Ix

Heme oxygenase (HO), a catabolic enzyme, provides the rate-limiting step in the oxidative breakdown of heme, to generate carbon monoxide (CO), iron, and biliverdin-IXα. Induction of the inducible form, HO-1, in tissues is generally regarded as a protective mechanism. Over the last decade, considerable progress has been made in defining the therapeutic potential of HO-1 in a number of preclinical models of lung tissue injury and disease. Likewise, tissue-protective effects of CO, when applied at low concentration, have been observed in many of these models. Recent studies have expanded this concept to include chemical CO-releasing molecules (CORMs). Collectively, salutary effects of the HO-1/CO system have been demonstrated in lung inflammation/acute lung injury, lung and vascular transplantation, sepsis, and pulmonary hypertension models. The beneficial effects of HO-1/CO are conveyed in part through the inhibition or modulation of inflammatory, apoptotic, and proliferative processes. Recent advances, however, suggest that the regulation of autophagy and the preservation of mitochondrial homeostasis may serve as additional candidate mechanisms. Further preclinical and clinical trials are needed to ascertain the therapeutic potential of HO-1/CO in human clinical disease.

Healing effects of curcumin nanoparticles in deep tissue injury mouse model.

2020 ◽  
Vol 18 ◽  
Author(s):  
Zirui Zhang ◽  
Shangcong Han ◽  
Panpan Liu ◽  
Xu Yang ◽  
Jing Han ◽  
...  
Keyword(s):  
Wound Healing ◽  
Mrna Expression ◽  
Tissue Injury ◽  
Inflammatory Cells ◽  
Pcr Analysis ◽  
Protective Effects ◽  
Deep Tissue ◽  
Deep Tissue Injury

Background: Chronic inflammation and lack of angiogenesis are the important pathological mechanisms in deep tissue injury (DTI). Curcumin is a well-known anti-inflammatory and antioxidant agent. However, curcumin is unstable under acidic and alkaline conditions, and can be rapidly metabolized and excreted in the bile, which shortens its bioactivity and efficacy. Objective: This study aimed to prepare curcumin-loaded poly (lactic-co-glycolic acid) nanoparticles (CPNPs) and to elucidate the protective effects and underlying mechanisms of wound healing in DTI models. Methods: CPNPs were evaluated for particle size, biocompatibility, in vitro drug release and their effect on in vivo wound healing. Results : The results of in vivo wound closure analysis revealed that CPNP treatments significantly improved wound contraction rates (p<0.01) at a faster rate than other three treatment groups. H&E staining revealed that CPNP treatments resulted in complete epithelialization and thick granulation tissue formation, whereas control groups resulted in a lack of compact epithelialization and persistence of inflammatory cells within the wound sites. Quantitative real-time PCR analysis showed that treatment with CPNPs suppressed IL-6 and TNF-α mRNA expression, and up-regulated TGF-β, VEGF-A and IL-10 mRNA expression. Western blot analysis showed up-regulated protein expression of TGF-β, VEGF-A and phosphorylatedSTAT3. Conclusion: Our results showed that CPNPs enhanced wound healing in DTI models, through modulation of the JAK2/STAT3 signalling pathway and subsequent upregulation of pro-healing factors.

scholarly journals The Potential Use of Vitamin C to Prevent Kidney Injury in Patients with COVID-19

Diseases ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 46
Author(s):  
Feng Xu ◽  
Yawei Wen ◽  
Xinge Hu ◽  
Tiannan Wang ◽  
Guoxun Chen
Keyword(s):  
Vitamin C ◽  
Distress Syndrome ◽  
Kidney Injury ◽  
Mortality Rates ◽  
Protective Effects ◽  
Global Public Health ◽  
Health Crisis ◽  
Public Health Crisis ◽  
Renal Functions ◽  
Potential Use

The newly found SARS-CoV-2 has led to the pandemic of COVID-19, which has caused respiratory distress syndrome and even death worldwide. This has become a global public health crisis. Unfortunately, elders and subjects with comorbidities have high mortality rates. One main feature of COVID-19 is the cytokine storm, which can cause damage in cells and tissues including the kidneys. Here, we reviewed the current literature on renal impairments in patients with COVID-19 and analyzed the possible etiology and mechanisms. In addition, we investigated the potential use of vitamin C for the prevention of renal injury in those patients. It appears that vitamin C could be helpful to improve the outcomes of patients with COVID-19. Lastly, we discussed the possible protective effects of vitamin C on renal functions in COVID-19 patients with existing kidney conditions.

scholarly journals Exogenous Surfactant Therapy for Pediatric Patients with Acute Respiratory Distress Syndrome

1997 ◽  
Vol 4 (1) ◽  
pp. 21-26 ◽  
Author(s):  
James F Lewis ◽  
Jasvinder S Dhillon ◽  
Ram N Singh ◽  
Craig C Johnson ◽  
Timothy C Frewen
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Pilot Study ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pediatric Patients ◽  
Distress Syndrome ◽  
Exogenous Surfactant ◽  
Lung Dysfunction ◽  
Surfactant Administration ◽  
Severe Lung

Exogenous surfactant administration is currently being tested in patients with the acute respiratory distress syndrome (ARDS). The results of the studies have varied because several factors may influence the host’s response to this therapy. This clinical pilot study was designed to evaluate the safety and efficacy of exogenous surfactant administration in pediatric patients with ARDS. Surfactant was administered to 13 patients with severe lung dysfunction, and eight of these patients experienced a significant improvement in oxygenation after the first dose of surfactant. In these patients the exogenous surfactant was administered within 48 h of the diagnosis of ARDS, whereas in the five patients who did not respond, surfactant was administered several days after the onset of ARDS. Responders also spent fewer days on a mechanical ventilator and less time in intensive care compared with nonresponders. Based on the results of this pilot study, a more appropriate multicentre clinical trial should be designed to evaluate this treatment strategy.

Oestrogen protects against ischaemic acute renal failure in rats by suppressing renal endothelin-1 overproduction

2002 ◽  
Vol 103 (s2002) ◽  
pp. 434S-437S ◽  
Author(s):  
Masanori TAKAOKA ◽  
Mikihiro YUBA ◽  
Toshihide FUJII ◽  
Mamoru OHKITA ◽  
Yasuo MATSUMURA
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Dysfunction ◽  
Tissue Injury ◽  
Male Rats ◽  
Left Renal Artery ◽  
Protective Effects ◽  
Endothelin 1 ◽  
Ischaemia Reperfusion

We investigated whether the treatment with 17β-oestradiol has renal protective effects in male rats with ischaemic acute renal failure (ARF). We also examined if the effect of 17β-oestradiol is accompanied by suppression of enhanced endothelin-1 production in postischaemic kidneys. Ischaemic ARF was induced by clamping the left renal artery and vein for 45min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function parameters such as blood urea nitrogen, plasma creatinine and creatinine clearance were measured to test the effectiveness of the steroid hormone. Renal function in ARF rats markedly decreased 24h after reperfusion. The ischaemia/reperfusion-induced renal dysfunction was dose-dependently improved by pretreatment with 17β-oestradiol (20 or 100µg/kg, intravenously). Histopathological examination of the kidney of untreated ARF rats revealed severe lesions, such as tubular necrosis, proteinaceous casts in tubuli and medullary congestion, all of which were markedly improved by the higher dose of 17β-oestradiol. In addition, endothelin-1 content in the kidney after the ischaemia/reperfusion increased significantly by approx. 2-fold over sham-operated rats, and this elevation was dose-dependently suppressed by the 17β-oestradiol treatment. These results suggest that oestrogen exhibits protective effects against renal dysfunction and tissue injury induced by ischaemia/reperfusion, possibly through the suppression of endothelin-1 overproduction in postischaemic kidneys.

scholarly journals Protective Effects of Taraxacum officinale L. (Dandelion) Root Extract in Experimental Acute on Chronic Liver Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 504
Author(s):  
Iulia Olimpia Pfingstgraf ◽  
Marian Taulescu ◽  
Raluca Maria Pop ◽  
Remus Orăsan ◽  
Laurian Vlase ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Failure ◽  
Tissue Injury ◽  
Taraxacum Officinale ◽  
Chronic Liver ◽  
Root Extract ◽  
Protective Effects ◽  
Stress Tests ◽  
Chronic Liver Failure

Background: Taraxacum officinale (TO) or dandelion has been frequently used to prevent or treat different liver diseases because of its rich composition in phytochemicals with demonstrated effect against hepatic injuries. This study aimed to investigate the possible preventing effect of ethanolic TO root extract (TOERE) on a rat experimental acute on chronic liver failure (ACLF) model. Methods: Chronic liver failure (CLF) was induced by human serum albumin, and ACLF was induced in CLF by D-galactosamine and lipopolysaccharide (D-Gal-LPS). Five groups (n = 5) of male Wistar rats (200–250 g) were used: ACLF, ACLF-silymarin (200 mg/kg b.w./day), three ACLF-TO administered in three doses (200 mg, 100 mg, 50 mg/kg b.w./day). Results: The in vivo results showed that treatment with TOERE administered in three chosen doses before ACLF induction reduced serum liver injury markers (AST, ALT, ALP, GGT, total bilirubin), renal tests (creatinine, urea), and oxidative stress tests (TOS, OSI, MDA, NO, 3NT). Histopathologically, TOERE diminished the level of liver tissue injury and 3NT immunoexpression. Conclusions: This paper indicated oxidative stress reduction as possible mechanisms for the hepatoprotective effect of TOERE in ACLF and provided evidence for the preventive treatment.

Evidence suggesting a role for hydroxyl radical in glycerol-induced acute renal failure

1988 ◽  
Vol 255 (3) ◽  
pp. F438-F443 ◽  
Author(s):  
S. V. Shah ◽  
P. D. Walker
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Hydroxyl Radical ◽  
Tissue Injury ◽  
Iron Chelator ◽  
Radical Scavenger ◽  
Reactive Oxygen Metabolites ◽  
Protective Effects ◽  
Hydroxyl Radical Scavenger ◽  
Hydroxyl Radical Scavengers

Reactive oxygen metabolites, in particular hydroxyl radical, have been shown to be important mediators of tissue injury in several models of acute renal failure. The aim of the present study was to examine the role of hydroxyl radical in glycerol-induced acute renal failure, a model for myoglobinuric renal injury. Rats injected with glycerol alone (8 mg/kg im following dehydration for 24 h) developed significant renal failure compared with dehydrated controls. Rats treated with glycerol and a hydroxyl radical scavenger, dimethylthiourea (DMTU), had significantly lower blood urea nitrogen (BUN) and creatinine. In contrast, urea, which is chemically similar to DMTU but is not a hydroxyl radical scavenger, provided no protection. In addition, DMTU prevented the glycerol-induced rise in renal cortical malondialdehyde content (a measure of lipid peroxidation that serves as a marker of free radical-mediated tissue injury). A second hydroxyl radical scavenger, sodium benzoate, had a similar protective effect on renal function (as measured by both BUN and creatinine). Because the generation of hydroxyl radical in biological systems requires the presence of a trace metal such as iron, we also examined the effect of the iron chelator, deferoxamine on glycerol-induced renal failure. Deferoxamine was also protective. The interventional agents were also associated with a marked reduction in histological evidence of renal damage. The protective effects of two hydroxyl radical scavengers as well as an iron chelator implicate a role for hydroxyl radical in glycerol-induced acute renal failure.

scholarly journals α-Crystallin B prevents apoptosis after H2O2 exposure in mouse neonatal cardiomyocytes

2012 ◽  
Vol 303 (8) ◽  
pp. H967-H978 ◽  
Author(s):  
Roxana Chis ◽  
Parveen Sharma ◽  
Nicolas Bousette ◽  
Tetsuaki Miyake ◽  
Aaron Wilson ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Cardiac Tissue ◽  
Small Heat Shock Protein ◽  
Subcellular Fractionation ◽  
Cellular Level ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Neonatal Cardiomyocytes ◽  
Caspase 12 ◽  
Voltage Dependent

α-Crystallin B (cryAB) is the most abundant small heat shock protein in cardiomyocytes (CMs) and has been shown to have potent antiapoptotic properties. Because the mechanism by which cryAB prevents apoptosis has not been fully characterized, we examined its protective effects at the cellular level by silencing cryAB in mouse neonatal CMs using lentivector-mediated transduction of short hairpin RNAs. Subcellular fractionation of whole hearts showed that cryAB is cytosolic under control conditions, and after H2O2 exposure, it translocates to the mitochondria. Phosphorylated cryAB (PcryAB) is mainly associated with the mitochondria, and any residual cytosolic PcryAB translocates to the mitochondria after H2O2 exposure. H2O2 exposure caused increases in cryAB and PcryAB levels, and cryAB silencing resulted in increased levels of apoptosis after exposure to H2O2. Coimmunoprecipitation assays revealed an apparent interaction of both cryAB and PcryAB with mitochondrial voltage-dependent anion channels (VDAC), translocase of outer mitochondrial membranes 20 kDa (TOM 20), caspase 3, and caspase 12 in mouse cardiac tissue. Our results are consistent with the conclusion that the cardioprotective effects of cryAB are mediated by its translocation from the cytosol to the mitochondria under conditions of oxidative stress and that cryAB interactions with VDAC, TOM 20, caspase 3, and caspase 12 may be part of its protective mechanism.

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