133 Oxidative Stress Can Be Significantly Influenced and Reduced by Polylactide-based Membrane Dressings

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S89-S89
Author(s):  
Herbert Haller ◽  
Mehmet Demircan ◽  
Kubilay Gurunluoglu

Abstract Introduction Oxidative stress is part of the physiological response to local thermal injuries and has systemic effects in more extensive burns, vascular hyperpermeability, burn edema, cellular damage, and functions of the heart, lung, liver, kidneys, muscles, and other organs. Free NO and OH radicals affect mitochondrial function, and lower energy delivery to other organelles releases thermal energy, leading to hypermetabolism. Antioxidant therapies have attempted to reduce the consequences of oxidative stress with limited effects; however, the effect of external dressings is unclear. This study aimed to investigate the positive effects of polylactide-based membranes (PLM) on oxidative stress and clinical outcomes in burns. Methods Herein, a prospective study assessed the correlation between oxidative stress and the severity of injuries by measuring serum malonaldehyde (MDA) and glutathione levels and the total oxidant and antioxidant capacities (TOC and TAC) among children with electrical injuries. Furthermore, a prospective randomized study evaluated the TOC and TAC, MDA, glutathione, IL-6, TNF-α, and TGF-β levels, and the ratio of telomerase positive staining in epidermal cells along the particle thickness of burns in children, when comparing polylactide dressings to Hydrofiber Ag(HFAg), autografts, and controls. Results Coherence between measured oxidative stress and injury severity was apparent herein. Application of PLMs significantly reduced oxidative stress in partial-thickness burns compared to HFAg. PLMs decreased the TOC (4,91 VS. 16,78 µmol/L, day 7) and increased the TAC (14,47 VS. 4,34 µmol/L, day 7). The healing duration was lesser than that of HFAg (13 VS. 21 d). Proinflammatory IL-6 levels were significantly lower in the PLM group and TNF-α values were significantly reduced from days 7 to 14. The anti-inflammatory levels of TGF-β was significantly elevated (days 3–21) in the PLM Group. Telomerase levels and the cell count were higher in healed skin in the PLM group. Conclusions Oxidative stress depends on injury severity and is potentially influenced by dressings. PLM mediates the regulation of oxidative stress, as evident from the TOC and TAC, and pro- and anti-inflammatory cytokines including IL-6, TNF-α, and TGF-β by PLMs might positively influence the healing duration and skin quality in burns. These results could show that oxidative stress can be significantly influenced and reduced by PLM dressings.

Author(s):  
Mamdooh Ghoneum ◽  
Mohamed S. A. El-Gerbed

Abstract Purpose Methotrexate (MTX) induces hepatotoxicity, limiting its clinical efficacy as a widely known chemotherapy drug. In the current study, we examined the protective effect of human placenta extract (HPE) against MTX-induced liver damage in rats, as well as its ability to regulate antioxidative and anti-inflammatory liver responses. Methods Male rats were orally administered MTX at a daily dose of 5 mg/kg-body-weight in the presence or absence of HPE (10.08 mg/kg) for 2 weeks. We measured the biological effects of MTX and HPE on the levels of liver enzymes, lipid profile, lipid peroxidation, oxidative stress biomarkers, and cytokines [tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10)]. In addition, histological examination and histopathological scoring of liver tissues were performed. Results MTX-treated rats showed significantly increased (p < 0.001) liver enzyme levels for aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, total cholesterol, and triglyceride levels. However, HPE supplementation in MTX-treated rats significantly decreased (p < 0.001) these elevated levels. HPE supplementation also significantly reduced the oxidative stress biomarker malondialdehyde (MDA), reversed the reduction in glutathione (GSH), and markedly increased the antioxidant enzyme activities of catalase (CAT) and superoxide dismutase (SOD) in the livers of MTX-treated rats. Furthermore, HPE supplementation significantly decreased the MTX-elevated levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-10. Histopathological examinations showed that MTX produced severe cellular damage and inflammatory lesions in liver tissues, while treatment with HPE improved hepatic histologic architecture. Conclusion HPE has the ability to ameliorate methotrexate-induced liver injury in rats by mechanisms that include boosting antioxidative responses and down-regulating MDA and pro-inflammatory cytokine production.


Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 985 ◽  
Author(s):  
Abdelhafid Nani ◽  
Babar Murtaza ◽  
Amira Sayed Khan ◽  
Naim Akhtar Khan ◽  
Aziz Hichami

Nutrition transition can be defined as shifts in food habits, and it is characterized by high-fat (chiefly saturated animal fat), hypercaloric and salty food consumption at the expense of dietary fibers, minerals and vitamins. Western dietary patterns serve as a model for studying the impact of nutrition transition on civilization diseases, such as obesity, which is commonly associated with oxidative stress and inflammation. In fact, reactive oxygen species (ROS) overproduction can be associated with nuclear factor-κB (NF-κB)-mediated inflammation in obesity. NF-κB regulates gene expression of several oxidant-responsive adipokines including tumor necrosis factor-α (TNF-α). Moreover, AMP-activated protein kinase (AMPK), which plays a pivotal role in energy homeostasis and in modulation of metabolic inflammation, can be downregulated by IκB kinase (IKK)-dependent TNF-α activation. On the other hand, adherence to a Mediterranean-style diet is highly encouraged because of its healthy dietary pattern, which includes antioxidant nutraceuticals such as polyphenols. Indeed, hydroxycinnamic derivatives, quercetin, resveratrol, oleuropein and hydroxytyrosol, which are well known for their antioxidant and anti-inflammatory activities, exert anti-obesity proprieties. In this review, we highlight the impact of the most common polyphenols from Mediterranean foods on molecular mechanisms that mediate obesity-related oxidative stress and inflammation. Hence, we discuss the effects of these polyphenols on a number of signaling pathways. We note that Mediterranean diet (MedDiet) dietary polyphenols can de-regulate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) and NF-κB-mediated oxidative stress, and metabolic inflammation. MedDiet polyphenols are also effective in upregulating downstream effectors of several proteins, chiefly AMPK.


2021 ◽  
Author(s):  
Yun Ding ◽  
Pengjie Tu ◽  
Yiyong Chen ◽  
Yangyun Huang ◽  
Xiaojie Pan ◽  
...  

Abstract Background Cytochrome P450 epoxygenase 2J2 (CYP2J2) metabolizes arachidonic acid to epoxyeicosatrienoic acids (EETs), which exert anti-inflammatory, anti-apoptotic, pro-proliferative, and antioxidant effects on the cardiovascular system. However, the role of CYP2J2 and EETs in pulmonary arterial hypertension (PAH) with lung ischemia-reperfusion injury (LIRI) remains unclear. In the present study, we investigated the effects of CYP2J2 overexpression and exogenous EETs on PAH with LIRI in vitro and in vivo.Methods CYP2J2 gene was transfected into rat lung tissue by recombinant adeno-associated virus (rAAV) to increase the levels of EETs in serum and lung tissue. A rat model of PAH with LIRI was constructed by tail vein injection of monocrotaline (50 mg/kg) for 4 weeks, followed by clamping of the left pulmonary hilum for 1 h and reperfusion for 2 h. In addition, we established a cellular model of human pulmonary artery endothelial cells (HPAECs) with TNF-α combined with hypoxic reoxygenation (anoxia for 8 h and reoxygenation for 16 h) to determine the effect and mechanism of exogenous EETs.Results CYP2J2 overexpression significantly reduced the inflammatory response, oxidative stress and apoptosis associated with lung injury in PAH with LIRI. In addition, exogenous EETs suppressed inflammatory response and reduced intracellular reactive oxygen species (ROS) production and inhibited apoptosis in a tumor necrosis factor alpha (TNF-α) combined hypoxia-reoxygenation model of HPAECs. Our further studies revealed that the anti-inflammatory effects of CYP2J2 overexpression and EETs might be mediated by PPARγ pathway; the anti-apoptotic effects might be mediated by the PI3K/Ak pathway.Conclusions CYP2J2 overexpression and EETs protect against PAH with LIRI via anti-inflammation, anti-oxidative stress and anti-apoptosis, suggesting that increased levels of EETs may be a promising strategy for the prevention and treatment of PAH with LIRI.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6565 ◽  
Author(s):  
Marie-Hélène Perruchot ◽  
Florence Gondret ◽  
Fabrice Robert ◽  
Emilien Dupuis ◽  
Hélène Quesnel ◽  
...  

Background High-yielding dairy cows are prone to oxidative stress due to the high metabolic needs of homeostasis and milk production. Oxidative stress and inflammation are tightly linked; therefore, anti-inflammatory and/or natural antioxidant compounds may help improve mammary cell health. Baicalin, one of the major flavonoids in Scutellaria baicalensis, has natural antioxidant and anti-inflammatory properties in various cell types, but its effects on bovine mammary epithelial cells (BMECs) have not been investigated. Methods Explants from bovine mammary glands were collected by biopsy at the peak of lactation (approximately 60 days after the start of lactation) (n = three animals) to isolate BMECs corresponding to mature secretory cells. Cell viability, apoptosis, proliferative capacity and reactive oxygen species (ROS) production by BMECs were measured after increasing doses of baicalin were added to the culture media in the absence or presence of H2O2, which was used as an in vitro model of oxidative stress. Results Low doses of baicalin (1–10 µg/mL) had no or only slightly positive effects on the proliferation and viability of BMECs, whereas higher doses (100 or 200 µg/mL) markedly decreased BMEC proliferation. Baicalin decreased apoptosis rate at low concentrations (10 µg/mL) but increased apoptosis at higher doses. ROS production was decreased in BMECs treated with increasing doses of baicalin compared with untreated cells, and this decreased production was associated with increased intracellular concentrations of catalase and NRF-2. Irrespective of the dose, baicalin pretreatment attenuated H2O2-induced ROS production. Discussion These results indicate that baicalin exerts protective antioxidant effects on bovine mammary cells. This finding suggests that baicalin could be used to prevent oxidative metabolic disorders in dairy cows.


Author(s):  
Sanjay Srinivasa ◽  
Santhosh K. Madhusudhan

Background: Chronic Kidney Disease (CKD) is one of the major health disorders associated with significant morbidity and mortality. This was a 6 week’s interventional study of orally administered, symbiotic supplement (probiotic with prebiotic) in stage 5D patients of chronic kidney disease (CKD) on twice a week hemodialysis. The objective was to look for safety of symbiotics (Nitrophage ForteTM) and for its anti-inflammatory effects measured by serum hsCRP (Highly specific C reactive protein), IL-6 (Interleukin- 6) and TNF-α (Tumour Necrosis Factor- α) levels. This translating to improvement in the Quality of life (QOL) assessed using SF-36 QOL questionnaire and Subjective Global Assessment (SGA) scoring. Methods: Subjects on twice a week dialysis for at least 3 months were included. Parameters at baseline (representing previous 3 months) were compared to that at the end of treatment. Oral supplementation of strain specific and unique composition of symbiotic sachet supplementation were administered twice daily containing Lactobacillus acidophilus 400mg, Bifidobacterium longumm 400mg, Streptococcus thermophilus with Fructooligosaccharide 100mg adding to 1 gram was given for 6 weeks.Results: 38 patients out of total 48 enrolled completed the study. Symbiotic therapy was found to be well tolerated with no significant adverse effects. 60.52%, 55.26%, 44.7% of the patients had a decrease in hsCRP, TNF-α and IL-6 respectively. Among responders hsCRP and TNF-α showed significant decrease in levels from the baseline (p <0.05). Modified SF-36 QOL questionnaire mean score revealed significant improvement in general health (p < 0.05). Among secondary parameters renal biomarkers like urea, BUN and sodium showed statistically significant decrease (p <0.05).Conclusions: This study establishes the safety and anti-inflammatory efficacy of this symbiotic supplement. To our knowledge this is the first study looking at anti-inflammatory role of symbiotic in CKD 5D Patients. A placebo controlled, double blinded study with a larger sample size is warranted in future to further establish these findings.


Author(s):  
Erkan Arslan ◽  
Hakan Turk ◽  
Murat Caglayan ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  

Background: Various effects of Astaxanthin was shown in the studies including its antioxidant, anti-inflammatory, anti-tumor and immunregulator effects. Objective: The aim of this study was to evaluate the beneficial effects of Astaxanthin on renovascular occlusion induced renal injury and to investigate the possible mechanisms. Methods: The rats were randomly assigned into three groups as follows: Group 1: control group (n=12), Group 2: renal ischemiareperfusion injury group (n=12), Group 3: renal ischemia-reperfusion + asthaxantine treated group (n=12). The control group and the renal ischemia-reperfusion group were given 2cc/kg/g olive oil for 7 days before establishing ischemia to renal tissue. Astaxanthin dissolved in olive oil was given orally to the renal ischemia+astaxanthin group for 7 days before inducing renal ischemia. Caspase-(3, 8, 9), GSH, SOD, Total Thiol, TNF-α, IL-6, 8-OHdG were performed for each group. Results: Renal IRI was verified by analysing the pathological changes of renal tissues and the renal functions after renal reperfusion. Much less renal tubular damage was determined the IRI+ASX group in comparison to the IRI group. Caspase-8, -9 and -3 immunoreactivity was observed to be minimal in the control group. Apoptosis was observed to be significantly reduced in the IRI + ASX group with respect to IRI group and close to the level of the control group (p <0.05). Caspase-3 levels of tissue samples were significantly increased in IRI group compared to other groups, but significantly lower in IRI+ASX group with respect to the IRI group (p<0.05). The TOS and OSI levels, indicating increased oxidative stress, were significantly lower in the IRI+ASX group with respect to the IRI group (p <0.001), but still higher than the control group (p <0.001). In addition to GSH, SOD and Total Thiol levels, TAS levels were also significantly higher in IRI + ASX group in comparison to the IRI group (p <0.05). TNF-α, IL-6, lipid hydroperoxide, AOPP and 8-OHdG levels were lower in the IRI+ASX group than the IRI group (p <0.001). MPO, IL-6, TNF-α levels, representing the parameters indicating neutrophil infiltration and inflammation of the renal tissues, significantly increased in IRI group with respect to the other groups (p <0.005). Conclusion: When all the data obtained in our study were evaluated, ASX was determined to prevent renal damage due to renovascular occlusion to a great extent, through complex mechanisms involving antioxidant, anti-inflammatory and antiapopitotic effects. Biochemical, histological and oxidative stress parameters were improved due to ASX.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
M. E. Nadia ◽  
A. S. Nazrun ◽  
M. Norazlina ◽  
N. M. Isa ◽  
M. Norliza ◽  
...  

Osteoporosis is characterized by skeletal degeneration with low bone mass and destruction of microarchitecture of bone tissue which is attributed to various factors including inflammation. Women are more likely to develop osteoporosis than men due to reduction in estrogen during menopause which leads to decline in bone-formation and increase in bone-resorption activity. Estrogen is able to suppress production of proinflammatory cytokines such as IL-1, IL-6, IL-7, and TNF-α. This is why these cytokines are elevated in postmenopausal women. Studies have shown that estrogen reduction is able to stimulate focal inflammation in bone.Labisia pumila(LP) which is known to exert phytoestrogenic effect can be used as an alternative to ERT which can produce positive effects on bone without causing side effects. LP contains antioxidant as well as exerting anti-inflammatory effect which can act as free radical scavenger, thus inhibiting TNF-α production and COX-2 expression which leads to decline in RANKL expression, resulting in reduction in osteoclast activity which consequently reduces bone loss. Hence, it is the phytoestrogenic, anti-inflammatory, and antioxidative properties that make LP an effective agent against osteoporosis.


Planta Medica ◽  
2020 ◽  
Vol 86 (06) ◽  
pp. 376-386 ◽  
Author(s):  
Gabriela Achete de Souza ◽  
Sâmylla Vaz de Marqui ◽  
Júlia Novaes Matias ◽  
Elen Landgraf Guiguer ◽  
Sandra Maria Barbalho

Abstract Ginkgo biloba (GB) is one of the most widely used phytotherapeutic products in the world, and its extract has beneficial properties for the treatment of several pathologies, such as diabetic cardiomyopathy, neurodegenerative diseases, cataracts, hearing loss, myocardial lesion, hippocampus neuronal lesions, morphometry testicular changes, and liver damage. This review aims to investigate the effects of GB on diseases related to oxidative stress. Databases such as MEDLINE/PUBMED and EMBASE were consulted, and PRISMA guidelines were used to build the review. This plant has antioxidant properties since it regulates the expression of antioxidant enzymes positively and reduces reactive oxygen and nitrogen species, contributing to the reduction of lipid peroxidation. It also exhibits anti-inflammatory properties, inhibiting the expression of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. In animal models, the use of GB can show positive effects on brain damage, neurodegenerative diseases, myocardial injury, and renal and liver damage. In humans, the positive effects were shown in diabetes, metabolic syndrome, and ischemic colitis. These effects are due to the presence of compounds such as bilobalide, isoramnetina, quercetin, kaempferol, and ginkgolides A, B, and C. For these reasons, GB can be a low-cost alternative to the therapeutic approach of several pathologies since it acts in the prevention, treatment, and inhibition of several complications of common comorbidities.


Herz ◽  
2019 ◽  
Vol 45 (S1) ◽  
pp. 130-138 ◽  
Author(s):  
T. Yu ◽  
D. Dong ◽  
J. Guan ◽  
J. Sun ◽  
M. Guo ◽  
...  

Abstract Background Clinical research has demonstrated that alprostadil has an anti-inflammatory effect; however, to date, its molecular mechanisms remain unclear. This study aimed to examine the anti-inflammatory activity and related mechanisms of alprostadil in lipopolysaccharide (LPS)-treated H9c2 cells. Methods Cell morphology was observed under an inverted light microscope, while cell viability was assessed with the 3‑(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assays (ELISA) were conducted to study biochemical indicators of cellular damage, such as released lactate dehydrase (LDH) and troponin, and inflammatory cytokine levels including interleukin-1β (IL-1β), IL-6, IL-17, and tumor necrosis factor-α (TNF-α). The mRNA expression levels of Wnt5a, c‑jun N‑terminal kinase (JNK), and nuclear factor kappa B (NF-κB) were further investigated by real-time quantitative polymerase chain reaction (RT-PCR). The effects of alprostadil on the Wnt5a/JNK/NF-κB pathway in H9c2 cells was examined by Western blotting. Results Alprostadil increased the cell viability of LPS-stimulated H9c2 cells, reduced LDH and troponin production, and attenuated IL-1β, IL-6, IL-17, and TNF-α secretion. Moreover, alprostadil reduced the mRNA expression of Wnt5a, JNK, and NF-κB and decreased the expression of Wnt5a, NF-κB, and the ratio of p‑JNK/JNK in H9c2 cells treated with LPS. The siWnt5a or JNK inhibitor SP600125 significantly augmented the inhibitory effects of alprostadil on the Wnt5a/JNK/NF-κB pathway. Conclusion Our results show that alprostadil has anti-inflammatory effects and could attenuate LPS-induced injury in H9c2 cardiomyocytes via the Wnt5a/JNK/NF-κB pathway.


2017 ◽  
Vol 30 (4) ◽  
pp. 383-394 ◽  
Author(s):  
Thangavelu Soundara Rajan ◽  
Francesca Diomede ◽  
Placido Bramanti ◽  
Oriana Trubiani ◽  
Emanuela Mazzon

Neuronal cell death is a normal process during central nervous system (CNS) development and is also involved in the death of motor neurons in diverse spinal motor neuron degenerative diseases. Here, we investigated the neuroprotective effect of secretory factors released from human gingival mesenchymal stem cells (hGMSCs) in mechanically injured murine motor-neuron-like NSC-34 cells. The cells were exposed to scratch injury and the markers for apoptosis and oxidative stress were examined. Immunocytochemistry results showed that proapoptotic markers cleaved caspase-3 and Bax were elevated while anti-apoptotic protein Bcl-2 was suppressed in scratch-injured NSC-34 cells. Oxidative stress markers SOD-1, inducible nitric oxide synthase (iNOS), Cox-2, and proinflammatory cytokine tumor necrosis factor alpha (TNF-α) were activated. Conditioned medium (CM) derived from hGMSCs (hGMSC-CM) significantly blocked the cell death by suppressing SOD-1, iNOS, TNF-α, cleaved caspase-3, and Bax. Bcl-2 and anti-inflammatory cytokine anti-interleukin 10 (IL-10) were increased in hGMSC-CM-treated injured cells. Moreover, hGMSC-CM treatment upregulated neurotrophins anti-brain-derived neurotrophic factor (BDNF) and NT3. Western blot data of hGMSC-CM revealed the presence of neurotrophins nerve growth factor (NGF), NT3, anti-inflammatory cytokines IL-10, and transforming growth factor beta (TGF-β), suggesting their positive role to elicit neuroprotection. Our results propose that hGMSC-CM may serve as a simple and potential autologous therapeutic tool to treat motor neuron injury.


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