Linum corymbulosum Protects Rats against CCl4-Induced Hepatic Injuries through Modulation of an Unfolded Protein Response Pathway and Pro-Inflammatory Intermediates.

Liver fibrosis is a major pathological feature of chronic liver disease and effective therapies are limited at present. The present study focuses on the hepatoprotective potential of L. corymbulosum against carbon tetrachloride (CCl4)-induced liver damage in rats. Analysis of Linum corymbulosum methanol extract (LCM) using high-performance liquid chromatography (HPLC) revealed the presence of rutin, apigenin, catechin, caffeic acid and myricetin. CCl4 administration lowered (p < 0.01) the activities of antioxidant enzymes and reduced glutathione (GSH) content as well as soluble proteins, whereas the concentration of H2O2, nitrite and thiobarbituric acid reactive substances was higher in hepatic samples. In serum, the level of hepatic markers and total bilirubin was elevated followed by CCl4 administration. The expression of glucose-regulated protein (GRP78), x-box binding protein-1 total (XBP-1 t), x-box binding protein-1 spliced (XBP-1 s), x-box binding protein-1 unspliced (XBP-1 u) and glutamate-cysteine ligase catalytic subunit (GCLC) was enhanced in CCl4-administered rats. Similarly, the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemo attractant protein-1 (MCP-1) was strongly increased with CCl4 administration to rats. Co-administration of LCM along with CCl4 to rats lowered (p < 0.05) the expression of the above genes. Histopathology of the liver showed hepatocyte injury, leukocyte infiltration and damaged central lobules in CCl4-treated rats. However, LCM administration to CCl4-intoxicated rats restored the altered parameters towards the levels of control rats. These outcomes indicate the existence of antioxidant and anti-inflammatory constituents in the methanol extract of L. corymbulosum.

Short to midterm follow-up of multi-system inflammatory syndrome in children with special reference to cardiac involvement.

OBJECTIVES: We aim to describe the early and upto 16 months follow-up of post-coronavirus disease (COVID), multi-system inflammatory syndrome in children (MIS-C), with special reference to cardiac involvement. STUDY DESIGN: This cohort non-interventional descriptive study included patients <18 years admitted between May, 2020 and April, 2021. Based on underlying similarities, children were classified as post-COVID MIS-C with overlapping Kawasaki Disease, MIS-C with no overlapping Kawasaki Disease, and MIS-C with shock. Post-discharge, patients were followed at 1, 3, 6, 12, and 16 months. RESULTS: Forty-one patients predominantly males (73%), at median age of 7 years (range 0.2-16 years) fulfilled the World Health Organisation criteria for MIS-C. Cardiac involvement was seen in 15 (36.5%); impaired left ventricle (LV) function in 5 (12.2%), coronary artery involvement in 10 (24.4%), pericardial effusion in 6 (14.6%) patients, and no arrhythmias. There were two hospital deaths (4.9%), both in MIS-C shock subgroup (2/10, 20%). At 1 month, there was persistent LV dysfunction in 2/5, coronary artery abnormalities in 7/10, and pericardial effusion resolved completely in all patients. By 6 months, LV function returned to normal in all but coronary abnormalities persisted in two patients. At last follow-up (median 9.8 months, interquartile range 2-16 months), in 36/38 (94.7%) patients, coronary artery dilatation was persistent in 2 (20%) patients. CONCLUSIONS: Children with MIS-C have a good early outcome, though MIS-C with shock can be life-threatening subgroup in a resource-constrained country setting. On midterm follow-up, there is normalisation of LV function in all and recovery of coronary abnormalities in 80% of patients.

Protective effects of vitexin on cadmium-induced renal toxicity in rats.

Cadmium (Cd) is an industrial contaminant that poses severe threats to human and animal health. Vitexin (VIT) is a polyphenolic flavonoid of characteristic pharmacological properties. We explored the curative role of vitexin on Cd-induced mitochondrial-dysfunction in rat renal tissues. Twenty-four rats were equally divided into four groups and designated as control, Cd, Cd + vitexin and vitexin treated groups. The results showed that Cd exposure increased urea and creatinine levels while decreased creatinine clearance. Cd reduced the activities of antioxidant enzymes, i.e., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione content in the Cd exposed group. Cd exposure significantly (p < 0.05) elevated the reactive oxygen species (ROS) and Thiobarbituric acid reactive substances (TBARS) levels in rat kidney. Cd also caused a significant (p < 0.05) reduction in the mitochondrial TCA-cycle enzymes, including isocitrate dehydrogenase, succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, and malate-dehydrogenase activities. Besides, mitochondrial respiratory chain enzymes, including NADH-dehydrogenase, coenzyme Q-cytochrome reductase, succinic-coenzyme Q, and cytochrome c-oxidase activities were also decreased under Cd exposure. Cd exposure also damaged the mitochondrial membrane potential (MMP). However, VIT treatment potentially reduced the detrimental effects of Cd in the kidney of rats. In conclusion, our study indicated that the VIT could attenuate the Cd-induced renal toxicity in rats.