Sericin ameliorated dysmorphic mitochondria in high-cholesterol diet/streptozotocin rat by antioxidative property

Abstract

The present work provides new insights regarding the antioxidative effect of sericin in (i) reducing blood cholesterol, (ii) improving liver and heart mitochondrial structures, (iii) maintaining endoplasmic reticulum integrity in exocrine pancreatic glands, and (iv) inhibiting fat deposition in the liver. Electron microscopic, histopathologic, immunohistochemical, and biochemical studies were performed. All of the results demonstrate the efficacy of sericin as a candidate for development of a functional food or adjunctive therapeutic agent against non-communicable diseases such as hypercholesterolemia. AbstractSericin has been implicated in lower cholesterolemic effect due to its properties with several mechanisms. Mitochondria are one of the most important targets to be affected in high blood cholesterol and glucose conditions. The protective role of sericin on mitochondria remains doubtful. To examine this role, electron microscopic, histopathologic, immunohistochemical, and biochemical studies were performed in a high-cholesterol diet/streptozotocin rat model. The results demonstrated that sericin reduced blood cholesterol without hypoglycemic effect. Sericin alleviated dysmorphic mitochondria in heart and liver but not in kidney and also decreased peculiar endoplasmic reticulum in the exocrine pancreas. In addition, sericin decreased hepatic steatosis and preserved zymogen granule referable to the decline of reactive oxygen species production in hepatic mitochondrial extraction and down-regulation of malondialdehyde expression in the liver and exocrine pancreas however irrelevant to lipase activity. This study suggests that sericin has antioxidative property to reduce blood cholesterol by means of diminishing fat deposit in hepatocyte and improves mitochondria and endoplasmic reticulum integrities.

Adaptive effect of sericin on hepatic mitochondrial conformation through its regulation of apoptosis, autophagy and energy maintenance: a proteomics approach

“…In agreement with our previous report indicating anti-oxidative properties of sericin in the heart and liver mitochondria, as shown by oxidative stress markers (e.g. superoxide dismutase, MDA and NRF-2) 1 , 2 , the present proteomics study confirmed that sericin preserves liver mitochondria from oxidative stress by maintaining ACO2 and CPT-II functions.…”

“…Several mechanisms, mainly focussing on competitive effects on cholesterol absorption, retardation of lipidogenesis in the liver and anti-oxidative properties, have been postulated. Our recent studies 1 , 2 have demonstrated that sericin improves dyslipidaemia and liver or heart mitochondrial architecture via its anti-oxidative activity, as characterised by the reduction in mitochondrial reactive oxygen species, downregulation of malondialdedhyde (MDA) and upregulation of nuclear factor erythroid 2-related factor (NRF-2). In addition, sericin increases lipase activity by enhancing pancreatic and adrenal gland biosynthesis via aquaporin-1 and tubulib-4β proteins.…”

Exogenous carbon monoxide protects against mitochondrial DNA‑induced hippocampal pyroptosis in a model of hemorrhagic shock and resuscitation

“…Mitochondria extraction and electron microscopy. The mitochondria from the hippocampal tissues were extracted 12 h after HSR (n= 6 per group) (17). Briefly, the hippocampal tissue homogenates were centrifuged twice at 1,000 x g and 4˚C for 5 min, and the supernatant was centrifuged at 15,000 x g and 4˚C for 2 min.…”

Streptozotocin induces alpha-2u globulin nephropathy in male rats during the end-stage of diabetic kidney disease

“…4). These findings likely indicate that increases in AQP- According to mitochondrial function and its architecture, mitochondrial dysfunction is a crucial factor in the pathogenesis of diabetic kidney diseases regarding reactive oxygen species overproduction, apoptosis activation and mitophagy defects [28][29][30][31][32][33][34]. The kidney is an extreme oxygen consumption organ, which renders it sensitive to mitochondrial dysfunction.…”

“…Consequent to the acclimatisation period, all rats were fasted for 6 h before being intraperitoneally infected with a single dose of 45 mg/kg streptozotocin (Sigma-Aldrich, USA) in fresh 0.1 M citrate buffer, pH 4.0 to induce hyperglycaemia [34]. Fasting blood glucose was examined in all of the rats, and a blood sugar level of ≥200 mg/dL was considered diabetic stage.…”