Effect of ozone therapy on oxidative stress indices in chronic inflammatory diseases: A systematic review and meta-analysis of randomized clinical trials

Effect of Ozone Therapy on Epidural Fibrosis in Rats

To evaluate the effectiveness of topical ozone therapy as an adjuvant treatment in the healing of lower limb ulcers through a systematic literature review. Three databases were used to search for studies conducted in the period up to and including September 2020: PubMed, Scopus, and the Web of Science. The search identified 44 studies, 7 of which met the eligibility criteria and were evaluated. Study design, study location, number of patients, patient age, type of control, wound type, intervention type, equipment used to generate ozone (ozone generation), evaluation methodology, and main results were extracted from each study. A total of 506 patients 18 years or older with chronic wounds, such as venous or diabetic ulcers, on the lower limbs were enrolled. The majority of studies addressed diabetic foot ulcers. The ozone therapy protocols demonstrated a healing effect in all included studies, and none reported adverse effects. This reinforces the need for more controlled and randomized clinical trials to determine the effectiveness of this treatment and establish clinical criteria for its use.

Effect of intrauterine ozone therapy on Asherman syndrome, an experimental rat model

Effects of ozone therapy on haemostatic and oxidative stress index in coronary artery disease

The objective: to evaluate the outpatient treatment of chronic pelvic inflammatory diseases of fertile aged women caused by mixed infection, including Chlamydia. Patients and methods. We examined 100 women chronic pelvic inflammatory diseases determining vaginal microbiota condition before and after treatment. Provided research of efficiency in the treatment of drug containing ciprofloxacin – and ornidazole 500 mg – 500 mg (Ortsypol) in women with chronic pelvic inflammatory diseases in lower levels of genital tract. Analysis of the vaginal bacterial spectrum and records of the results was performed according to the order number 234 of the Ministry of Health of Ukraine 2005 Results. Our results have shown that most women suffered from chronic pelvic inflammatory diseases in lower level of genital tract during one year (30%), slightly less women had disease duration of 3 years (27%) and 5 years (25%). Among other gynecological diseases in examined women often diagnosed cervical erosion (14%) and the polycystic ovarian syndrome (18%). Often diagnosed ovarian cysts (10%), endometriosis (11%) and endometrial hyperplasia (9%). Examination of vaginal mikrobiome in fertile aged women with chronic pelvic inflammatory diseases showed increased number of resident microflora and STIs, mainly: Chlamidya trahomatis (25%), Ureaplasma urealiticum (23%). We observed significant reduction of the number of pathogenic and conditionally pathogenic microflora in fertile aged women with chronic pelvic inflammatory diseases after treatment rizke. Conclusion. 1. The most common cause of vaginal dysbiosis in women that were attending outpatient clinic, were sexually transmitted infections, among which most commonly we diagnosed Chlamidya trahomatis. 2. In the development of inflammatory reactions in reproductive organs and chronic pelvic inflammatory diseases main role plays microbial and viral and microbial associations in which Chlamidya trahomatis and Ureaplasma urealiticum are present. 3. Use of a complex chronic pelvic inflammatory diseases treatment of lower genital tract using Ortsypol shown to be highly effective (95%). Key words: chronic inflammatory diseases, fertile aged women, infections, sexually transmitted infections, outpatient treatment, Ortsypol.

Psoriasis vulgaris (PV), a chronic inflammatory skin disease, is a condition of increased oxidative stress (OxS). However, interest related to oxidative and carbonyl stress damages to proteins, such as the formation of advanced glycation end products (AGEs) and their precursor molecule methylglyoxal (MG) has been modest. The objective of this study was to compare the systemic levels of OxS markers in patients with PV and healthy controls (Co) and to investigate their correlation with the serum level of MG. Total peroxide concentration (TPX) and total antioxidant capacity (TAC) were estimated by means of spectrophotometry. The TPX and TAC ratio was regarded as OxS index (OSI). MG level was determined using ELISA. Compared to Co, patients with PV had significantly increased blood levels of TPX (P < 0.0001), OSI (P < 0.0001), and MG (P = 0.01), and lower TAC levels (P < 0.0001). Increase in body mass index (BMI) appeared to contribute to this imbalance as TAC levels decreased with increasing BMI (r = -0.252, P < 0.01). Increased TPX concentration was associated with higher serum level of MG (r = 0.610, P = 0.004), the latter being positively correlated with psoriasis area and severity index (r = 0.577, P = 0.008). In performed multivariate regression analysis, TPX, TAC, and OSI were all significant predictors of MG level. Our study gave further proof of increased systemic psoriasis-related OxS. MG serum level, reflecting simultaneously OxS as well as carbonyl stress status, could be used as a marker of disease activity in clinical trials while looking for new systemic therapies for psoriasis.

Recommendations for assessing the risk of cardiovascular disease and venous thromboembolism before the initiation of targeted therapies for chronic inflammatory rheumatic diseases.

Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p=0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p=0.005 and p=0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p=0.6; p=0.4 and p=0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.

Atherosclerosis is a chronic vascular inflammatory disease associated to oxidative stress and endothelial dysfunction. It is characterized by lipid accumulation in the arterial wall, increased hyperlipidemia, oxidative stress, lipid peroxidation, and protein oxidation. Our study included 45 patients ages of 40–60 and 45 healthy volunteers with similar demographic characteristics without any chronic disease as well. Fasting plasma glucose, BUN, creatinine, LDL-cholesterol, HDL-cholesterol, triglyceride, total cholesterol, HbA1c, and C-reactive protein (CRP) levels were measured using commercial kits by autoanalyzer. The oxidative stress biomarkers total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), native thiol (NT), catalase (CAT), paraoxonase (PON1), and arylesterase (ARES) enzyme activities were measured using photometric methods. The inflammatory biomarkers interleukin 1 beta (IL-1β), tumor necrosis factor-α (TNF-α), presepsin (PSPN), and raftlin (RFTN1) levels were measured with ELISA Kits. Oxidative stress index (OSI) and disulfide (DIS) were calculated. The clinical, biochemical biomarkers such as BUN, creatinine, HDL, LDL, total cholesterol, triglyceride, and CRP levels were found to be higher than the control group and lower post-treatment compared to the pre-treatment group (p <0.001). The oxidative stress parameters, TOS, OSI, and DIS levels were found to be higher than the control group, and the levels before the treatment were statistically significantly higher than after the treatment (p < 0.001).Antioxidant biomarkers TAS, TT, and NT levels were low in the patient group. Inflammatory biomarkers were highest before treatment and decreased with treatment. Oxidative stress and inflammation, which increased in atherosclerosis patients may guide disease prognosis and treatment strategies.

ABSTRACTPurpose: The purpose of this study was to investigate (a) time-dependent changes in muscle damage (MD) biomarkers, oxidative stress (OS) indices, and maximum strength performance; (b) the relationship between changes in maximum strength performance and changes in MD and OS indices; and (c) whether eccentric exercise-induced MD is related to OS. Method: Twenty-nine male volunteers (age: 22.13 ± 3.1 years) participated in the study. Participants performed 60 maximal eccentric actions of the elbow flexors at a constant velocity of 60°·s−1. Maximum isokinetic strength (MIS), visual analog scale soreness scores, serum creatine kinase (CK) activity, total antioxidant status, total oxidant status (TOS), protein carbonyl (PCO), and 8-hydroxydeoxyguanosine level were analyzed. Blood samples were obtained before, immediately after, and 24 h, 48 h, and 96 h after the eccentric exercise. Change in total work (%ΔTWk), peak torque (%ΔPT), and OS index were calculated. Results: CK, PCO, and TOS significantly increased over time (p < .05). However, no significant main effect was observed for MIS or any other investigated biomarkers (p > .05). MIS was not related to MD or OS indices. However, %ΔTWk demonstrated a moderate inverse correlation with OS indices. No significant relationship was observed between %ΔPT and any of the selected biomarkers. Conclusions: Our findings confirm the hypothesis that acute eccentric exercise increases MD biomarkers and OS indices. However, indices of OS damage were significantly related, particularly, to the strength loss of flexors. This finding suggests that the decline in strength performance is not the primary determinant of the magnitude of MD following voluntary eccentric contraction.

Background and aimsMucous mesenchymal stem cells can migrate to damaged areas, and their use is proposed as a new approach to treating diseases. The present study aimed to investigate the effect of oral mesenchymal stem cells (OMSCs) on inflammatory, oxidative stress, and histopathological indices in the tissues of the stomach, intestine, and colon after traumatic brain injury (TBI).Methods and materialsAdult male rats were randomly divided into four groups: Sham, TBI, Vehicle (Veh), and Stem cell (SC). Intravenous injection of OMSCs was performed at 1 and 24 h after injury. The inflammatory, oxidative stress, and histopathological indices of the tissues of the stomach, small intestine, and colon were evaluated 48 h after injury.ResultsAfter TBI, IL-1β and IL-6 levels increased and IL-10 levels decreased in the tissues of the stomach, small intestine, and colon, but the administration of OMSCS prevented these changes to a large extent. Oxidative stress indices (MDA, PC, TAC, SOD, and CAT) showed an increase in oxidative stress after TBI, but oxidative stress was less severe in the OMSC group. The administration of OMSCs after TBI improved the histopathological outcome in the tissues of the stomach, small intestine, and colon.ConclusionAdministration of OMSCs in rats suffering from TBI can improve inflammatory, oxidative stress, and histopathological indices in the tissues of the stomach, small intestine, and colon, which shows the beneficial effect of using OMSCs in TBI.

Chronic diseases and conditions, such as kidney and liver failure, cancers, and diabetes, are the leading causes of morbidity and mortality, and, according to the data published by the World Health Organization [1], these diseases caused 38 million deaths in 2009 alone, more than 62% of all deaths around the world. However, the pathogenesis of these diseases is not fully understood yet. In more recent years, evidence indicates the link of a form of low-degree systemic and chronic inflammation to many types of chronic diseases including cancer [2–6], suggesting the inflammation as a common risk factor for these diseases. What is inflammation? The word inflammation comes from the Latin “inflammo,” meaning “blaze, burn,” and is defined in biology as “the body's immune system's response to stimulus” by the US National Library of Medicine. The inflammation is commonly ignited by the pathogen (bacteria, viruses, or fungi) infection, tissue injuries and remodeling, or nonphysiological cell death, and is typically viewed as a self-protective response and is important for wound healing. However, in most cases, prolonged or chronic inflammation leads to the pathological changes in body tissues or organs, an inflammatory disease. To understand how the inflammation contributes to the chronic diseases including cancer, we have collected eight clinical observation and experimental studies in this special issue focusing on the mediators of inflammation in chronic diseases and cancer. Using systemic review and meta-analysis, W. Wang et al. have shown an association of gout with an increased risk of cancer, particularly urological cancers, digestive system cancers, and lung cancer. Similarly, there is a positive correlation of serum uric acid levels with total cancer incidence, but it is only found in males not in females (S. Yan et al.). Gout is an inflammatory response to the accumulated urate crystals in the joint that may be formed due to the high levels of uric acid in the blood, in which uric acid crystals have been identified as an endogenous stimulus for activation of the immune responses, particularly interleukin-1β-mediated inflammation via activation of the NOD-like receptor protein 3 (NLRP3) inflammasome [7]. How this inflammatory response is related to tumor development and why this association is gender-dependent are not known. The association of a panel of inflammation mediators, such as interleukin-8 and tumor necrosis factor- (TNF-) α, with chronic diseases (liver disease and gastritis) and different types of cancer (liver and gastric cancer and melanoma) has been documented in this issue (T. Liu et al.; A. Essadik et al.; C.-D. Ene et al.). Whether upregulation of these mediators is part of pathogenesis of these diseases or is just an associated risk factor requires further investigation. Interestingly, T. Liu et al. summarize that c-Myc, a protooncogene, may play a central role in the development of liver inflammation as well as liver cancer. Is mutation of c-Myc required for the stimulation of inflammation in the liver? A similar question is for the study by A. Essadik et al.; whether the mutation at TNF-α−238 (G/A) allele found in patients with gastric pathologies promotes the transcription of TNF-α or that at TNF-α−193 (G/A) downregulates its expression needs further investigation. Finally, we do need well-designed experimental studies to answer our question, the role of inflammation in chronic diseases, carefully. G. C. W. Chan et al. present a good example for that by showing different effects from others in literature of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) or Captopril treatment on the attenuation of interstitial injury or macrophage in a mouse model of chronic kidney disease. In summary, chronic diseases including cancer somehow affect everyone's life, and we do not know the exact cause of these diseases and how to effectively treat or prevent them as of today. Numerous studies including the papers published in this issue clearly show the association of inflammation with the development of chronic diseases, but we have more questions about the role of inflammation in the pathogenesis of these diseases than the answers we have to that as of today. Caigan Du Madhav Bhatia Sydney C. W. Tang Mingzhi Zhang Theodore Steiner

The isoprostanes (IsoPs) are a unique series of prostaglandin-like compounds formed in vivo via a nonenzymatic mechanism involving the free radical-initiated peroxidation of arachidonic acid. This article summarizes our current knowledge of these compounds. Herein, a historical account of their discovery and the mechanism of their formation are described. A specific class of IsoPs, the F2-IsoPs, are stable, robust molecules that can be measured as indices of endogenous oxidant stress. The utility of these molecules as biomarkers and methods by which these compounds can be quantified are discussed. In addition to the F2-IsoPs, isoprostanes with other prostane ring structures as well as oxidation products with furan and dioxolane rings can be generated from arachidonic acid. And, in more recent years, isoprostane-like compounds have been shown to be formed from polyunsaturated fatty acids including eicosapentaenoic acid [C20:5, omega-3], docosahexaenoic acid [C22:6, omega-3], and adrenic acid [C22:4, omega-6]. These findings will be summarized as well.

Telomere shortening in chronic obstructive pulmonary disease

Vitamin C and E supplementation in women at risk of preeclampsia is associated with changes in indices of oxidative stress and placental function