Parkinson’s disease is a common movement disorder associated primarily with oxidative stress-mediated degeneration of dopaminergic neurons. Earlier studies showed that Sorghum bicolor-based supplement (SbS) exhibited antioxidant and neuroprotective activities and might likely rescue the death of dopaminergic neurons in Parkinson’s disease. This study examined the effect of SbS on rotenone-induced Parkinsonian-like motor deficits in rats and the involvement of oxidative stress and pro-inflammatory cytokines. Rats were divided into six groups and treated orally with sunflower oil (vehicle-control), rotenone (2.5 mg/kg) (...) alone or in combination with each dose of SbS (50, 100, and 200 mg/kg) and levodopa-carbidopa (10 mg/kg) on an alternate day for 28 days. The changes in motor functions were evaluated on day 28 and the brain concentrations of oxidative stress biomarkers and pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) were determined. Rotenone caused motor deficits by impaired locomotor activity in the open field test and induced catalepsy in the bar test, which were attenuated by SbS. Rats pretreated with SbS had reduced brain levels of malondialdehyde, nitrite, and pro-inflammatory cytokines compared to rotenone controls. SbS mitigated rotenone-induced depletion of reduced glutathione and antioxidant enzymes in the rat brain. The results suggest that SbS ameliorated rotenone-induced Parkinsonian-like motor dysfunctions by reducing neuronal oxidative stress and pro-inflammatory cytokines in rats. (shrink)

The environment can elicit biological responses such as oxidative stress (OS) and inflammation as a consequence of chemical, physical, or psychological changes. As population studies are essential for establishing these environment-organism interactions, biomarkers of OS or inflammation are critical in formulating mechanistic hypotheses. By using examples of stress induced by various mechanisms, we focus on the biomarkers that have been used to assess OS and inflammation in these conditions. We discuss the difference between biomarkers that are the result of a (...) chemical reaction (such as lipid peroxides or oxidized proteins that are a result of the reaction of molecules with reactive oxygen species) and those that represent the biological response to stress, such as the transcription factor NRF2 or inflammation and inflammatory cytokines. The high-throughput and holistic approaches to biomarker discovery used extensively in large-scale molecular epidemiological exposome are also discussed in the context of human exposure to environmental stressors. We propose to consider the role of biomarkers as signs and to distinguish between signs that are just indicators of biological processes and proxies that one can interact with and modify the disease process. (shrink)

Inflammation is activated by diverse triggers that induce the expression of cytokines and adhesion molecules, which permit a succession of molecules and cells to deliver stimuli and functions that help the immune system clear the primary cause of tissue damage, whether this is an infection, a tumor, or a trauma. During inflammation, short-term changes in the expression and secretion of strong mediators of inflammation occur, while long-term changes occur to specific groups of cells. Long-term changes include cellular transdifferentiation for (...) some types of cells that need to regenerate damaged tissue, as well as death for specific immune cells that can be detrimental to tissue integrity if they remain active beyond the boundaries of essential function. The transcriptional regulator NFκB enables some of the fundamental gene expression changes during inflammation, as well as during tissue development. During recurrence of malignant disease, cell stress-induced alterations enable the growth of cancer cell clones that are substantially resistant to therapeutic intervention and to the immune system. A number of those alterations occur due to significant defects in feedback signal cascades that control the activity of NFκB. Specifically, cell stress contributes to feedback defects as it overrides modules that otherwise control inflammation to protect host tissue. NFκB is involved in both the suppression and promotion of cancer, and the key distinctive feature that determines its net effect remains unclear. This paper aims to provide a clear answer to at least one aspect of this question, namely the mechanism that enables a divergent response of cancer cells to critical inflammatory stimuli and to cell stress in general. (shrink)

The public health crisis is started with emergence of new coronavirus on 11 February 2020 which triggered as coronavirus disease-2019 (COVID-19) pandemics. The causative agent in COVID-19 is made up of positively wrapped single-stranded RNA viruses ~ 30 kb in size. The epidemiology, clinical features, pathophysiology, and mode of transmission have been documented well in many studies, with additional clinical trials are running for several antiviral agents. The spreading potential of COVID-19 is faster than its two previous families, the severe (...) acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV). Apart from clinical manifestation, comorbid status is playing key role for prevalence of COVID-19 infection and mortalities. The comorbid effects associated with COVID-19 are diabetes, cardiovascular, digestive, hepatitis-B, cerebrovascular, hypertension, liver injury, coronary heart disease, cancer, rheumatoid arthritis, and neurological impairment. Antimalarial drugs (chloroquine and hydroxychloroquine), remdesivir, Tocilizumab, clopinavir/ritonavir, convalescent plasma therapy, spike protein-angiotensin-converting enzyme 2 (ACE2) inhibitors, human monoclonal antibodies, mRNA-1273, mesenchymal stem cells, Indian and Chinese traditional medicine, small molecules antioxidant, natural products and dietary supplements, high doses of vitamin-E, -C, -D, minerals, flavonoids,and IFN-beta are therapeutic intervention running to develop treatment against COVID-19. Although clinical usage of these therapeutic agents against COVID-19 is well documented, cytokine storms, absence of appropriate animal model have limited its therapeutic use. This review explores the clinical information currently available on COVID-19 on the mechanisms of infection, prevention, management, comorbid status, and current drug treatment options. (shrink)

Abstract: A complex parasite such as human Plasmodium is likely to generate a variety of substances that injure the hosts directly or cause immunopathology. In malaria, a blood concentration of anti-inflammatory cytokines, such as interleukin (IL-10) is increased. The present study was performed to analyze IL-10 levels in patients with malaria falciparum and healthy controls individuals and correlate with malaria density infection as well as age groups. It is a cross sectional study was carried out in Khartoum state /Sudan, (...) a total of 70 febrile patients and 20 healthy volunteers as controls were included in this study. Blood samples were collected from both patients and control candidates in (EDTA) containers for parasitological and immunological tests. Immunochromatography test and microscopic examination for both thick and thin blood films were used to detect the positive samples for Plasmodium falciparum. Enzyme linked Immunosorbant Assay (ELISA), was used for the determination of IL-10 levels. The result showed that of IL-10 levels in malaria patients were 1598.50 and SD 4771.64 while the levels in healthy participants the level was 10.39 and SD was 124.33 the difference was found to be statistically significant (P= 0.007). The levels of cytokines mentioned above were observed to be raised in malaria individual compared to healthy control candidates. (shrink)

Systemic juvenile idiopathic arthritis is classified as an autoimmune entity and a subtype of juvenile idiopathic arthritis, although it has many features of autoinflammatory-type of diseases. This review article will elaborate on the disease’s pathogenesis and its proposed relation to autoinflammatory diseases including defective innate immunity and phagocytosis response leading excessive cytokine release. It also explains the disease’s epidemiology, clinical phenotype, diagnostic challenges, complications and current advancements in the treatment of systemic juvenile idiopathic arthritis, such as IL-1 and IL-6 antagonists (...) and their impact on the disease trajectory. Care of patients with systemic juvenile idiopathic arthritis requires a comprehensive multidisciplinary team to optimize the care and avoid complications of the disease itself such as growth impairment, macrophage activation syndrome or the complications of immunosuppressant and immunomodulatory treatments. (shrink)