Highlights SARS-CoV-2 interfered primarily by angiotensin-converting enzyme 2 (ACE2) receptor. Depending on the viral load, SARS-COV-2 infections spread to other major organs, mainly based on ACE2 receptor expression. Cytokine storm and organ crosstalk result in systemic inflammation with multi-organ failure syndromes.

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Many controversial reports are available on the use of aspartame as it releases methanol as one of its metabolite during metabolism. The present study proposes to investigate whether long term (90 days) aspartame (40 mg/kg b.wt) administration could induce oxidative stress and alter the memory in Wistar strain male albino rats. To mimic the human methanol metabolism, methotrexate (MTX)-treated rats were included as a model to study the effects of aspartame. Wistar strain albino rats were administered with aspartame (40 mg/kg b.wt) orally and studied along with controls and MTX-treated controls. Aspartame interfered in the body weight and corticosterone levels in the rats. A marked increase in the mRNA and protein expression of neuronal nitric oxide synthase (nNOS) and induced nitric oxide synthase (iNOS) which resulted in the increased nitric oxide radical's level indicating that aspartame is a stressor. These reactive nitrogen species could be responsible for the altered cell membrane integrity and even cause death of neurons by necrosis or apoptosis. The animals showed a marked decrease in learning, spatial working and spatial recognition memory deficit in the Morris water maze and Y-maze performance task which could have resulted due to reduced hippocampal acetylcholine esterase (AChE) activity. The animal brain homogenate also revealed the decrease in the phosphorylation of NMDAR1-CaMKII-ERK/CREB signalling pathway, which well documents the inhibition of phosphorylation leads to the excitotoxicity of the neurons and memory decline. This effect may be due to methanol which may also activate the NOS levels, microglia and astrocytes, inducing neurodegeneration in brain. Neuronal shrinkage of hippocampal layer due to degeneration of pyramidal cells revealed the abnormal neuronal morphology of pyramidal cell layers in the aspartame treated animals. These findings demonstrate that aspartame metabolites could be a contributing factor for the development of oxidative stress in the brain.

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The objective of this study was to evaluate the free radical scavenging potential and high performance thin layer chromatography (HPTLC) fingerprinting of Indigofera tinctoria (I. tinctoria). Phytochemical analysis was carried out using standard methods, and free radical scavenging activity of the plant was determined using 2,2-diphenyl-1-picrylhydrazy (DPPH), nitric oxide (NO) and superoxide anion (normalO2−) radical scavenging capacities. HPTLC plate was kept in CAMAG TLC Scanner 3 and the Rf values at fingerprint data were recorded by WINCATS software. Aqueous extract of I. tinctoria reliably showed the total phenolics (267.2±2.42 mg/g), flavonoids (75.43±3.36 mg/g) and antioxidants (349.11±8.04 mg/g). The extract was found to have DPPH (52.08%), NO (23.12%) and normalO2− (26.79%) scavenging activities at the concentration of 250 μg/mL and the results were statistically significant compared with ascorbic acid standard (p<0.05). HPTLC results confirmed that the extract contained several potential active components such as phenols, flavonoids, saponins and terpenoids as the slides revealed multi-colored bands of varying intensities. This study confirmed that the plant had multipotential antioxidant and free radicals scavenging activities.

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The objective of the study is to evaluate the DNA damage, behavior and free radical scavenging enzymes level when exposed to noise. Noise stress was performed using broadband white noise generator after pre-treated oral administration of Indigofera tinctoria (300mg/Kg .b.w.). Significance increase in nitric oxide and lipid peroxidation level in stressed rat shows possibility of neurodegeneration and this is justified by genomic DNA damage in brain discrete region. Increase in enzymatic and decrease in non-enzymatic level suggest that oxidative imbalance persist in animal when expose to noise in both brain and adrenal. Anxiety and altered motor coordination was also observed in our studies, this finding could be attributed to the detrimental effects of noise not only at the biochemical level but also the molecular and psychological behavior of the rat. However, oral administration of I.tinctoria significantly prevented noise induced oxidative damages. These results conclude that I.tinctoria may possess neuroprotective effects and the antioxidant property of the plant may have resulted in its therapeutic efficacy.