Objective: There has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. The aim of this study is to investigate the existence of oxidative stress and inflammatory marker IL-8 in patients with acne vulgaris, and the role of oxidative stress as a therapeutic target in the treatment of acne vulgaris. Methods: A randomized prospective clinical trial was carried out on 56 patients of both sexes with age range of 14-35 years who attend to outpatient clinic in Al-Hussein Teaching Hospital-Kerbalaa-Iraq over a period from December 2011 to May 2012, all patients examined clinically by dermatologist and classified according to disease severity. Serum levels of glutathione (GSH), malondialdehyde (MDA) and interleukine-8 (IL-8) in the acne patients were measured by using ready-for-use Elisa kits, and compared to that of 28 healthy volunteers. Results: The results of the serum level analysis of MDA for the acne patients (expressed as the mean± standard deviation) was highly significant (P value ≤ 0.001) higher than that of healthy volunteers, while serum level of GSH was highly significant (P value ≤ 0.001) lower in acne patients compared to healthy volunteers; there is a significant difference (P value ≤ 0.05) found in serum levels of IL-8 between the acne patients and the healthy volunteers. Conclusions: The results obtained in this study clearly showed the existence of oxidative stress in patients with acne vulgaris, and that oxidative stress along with inflammation play a critical role in acne pathogenesis; furthermore, oxidative stress in acne patients may represents a potential therapeutic target and interference with antioxidant is a rationale choice.

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Background: A cytokine storm is a serious clinical condition that complicates infectious diseases, for example, coronavirus disease 2019 (COVID-19), and non-infectious diseases such as autoimmune diseases and cancer and may often lead to death. The patients who are affected by the cytokine storm are almost always severe/critical and at risk for acute respiratory distress syndrome or eventually death. Pro-inflammatory cytokines such as interleukin 6 (IL-6), IL-1 beta, and tumor necrosis factor alpha (TNF-α) have been repeatedly shown to be related to the COVID-19 disease severity and mortality. In this study, our objective was to evaluate the attenuated effect of rivastigmine (RA) in a cytokine storm in Swiss Albino mice in which the cytokine storm was induced by lipopolysaccharide (LPS) and to explore their effects on IL-1 β, IL-6, and TNF-α levels. Methods: This study was carried with 60 male Swiss albino mice that were divided equally and randomly into six groups as follows: • Group AH: Apparently healthy control group which received no induction, not treated. • Group LPS: Induced using LPS at 5 mg/kg and no treatment administered. • Group DMSO: Induced and treated with 1% dimethyl sulfoxide (DMSO). • Group RA: Induced and treated with 0.5 mg/kg RA. • Group MPA: Induced and treated with 50 mg/kg methylprednisolone (MPA). • Group RMPA: Induced and treated with 0.25 mg/kg rivastigmine and 25 mg/kg of methylprednisolone. All the mice were treated with drugs or vehicles for three consecutive days before LPS induction. The mice were then injected with LPS intraperitoneally at a dosage of 5 mg/kg for systematic inflammatory stimulation. After 48 hours of LPS induction, all the mice were euthanized by light anesthesia with chloroform, and blood was collected for the quantitative determination of IL-1β, IL-6, and TNF-α levels using the enzyme-linked immunosorbent assay (ELISA) technique. Results: Administration of LPS to Swiss albino mice caused a significant elevation of IL-1β, IL-6, and TNF-α levels than in the healthy control group. Significant reduction of these parameters were observed in the RA and MPA groups when compared with those in the non-treated group. Conclusion: RA was found to be effective in attenuating the induced cytokine storm by suppressing IL-1β, IL-6, and TNF-α levels, and the results with RA were comparable to that of MPA. A combination of half-doses of both RA and MPA administered together shows no obvious advantage when compared with that of each of them alone.

Ischemic reperfusion injury (IRI) of the kidneys is a direct sequela of surgical procedures associated with the interruption of blood supply. The pathophysiology of IRI is complicated, and several inflammatories, apoptosis, and oxidative stress pathways are implicated. Among the major receptors directly involved in renal IRI are the toll-like receptors (TLRs), specifically TLR2 and TLR4. In this study, we investigated the effects of Lipopolysaccharide from Rhodobacter Sphaeroides (TLR2 and TLR4 antagonist, LPS-RS) and the ultrapure form (pure TLR4 antagonist, ULPS-RS) on the histopathological changes and TLRs expression in an animal model of bilateral renal IRI. Forty-eight adult male rats were allocated into six groups (N=8) as follows: sham group (negative control without IRI), control group (rats underwent bilateral renal ischemia for 30 minutes and 2 hours of reperfusion), vehicle group (IRI+ vehicle), LPS-RS group (IRI+ 0.5 mg/kg of LPS-RS), ULPS-RS group (IRI+ 0.1 mg/kg of ULPS-RS), ULPS-RSH group (IRI+ 0.2 mg/kg of ULPS-RS). Significant improvement in the histopathological damages induced by renal IRI was found in the ULPS-RS treated groups at both doses compared with the control group. The protective effect of ULPS-RS was associated with significantly reduced TLR4 expression without affecting TLR2. Regarding LPS-RS, the tested dose adversely affected the renal tissues as manifested by the histopathological findings, although it similarly affected TLRs expression as ULPS-RS. Our results demonstrated that ULPS-RS was renoprotective while LPS-RS had no protective effect against the tissue damages induced by renal IRI.