ArticleEndocrine2015
Protective effect of Schisandrae chinensis oil on pancreatic β-cells in diabetic rats.
Article in Endocrine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 15 citations in OpenAlex.
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Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Islet cell dysfunction in type 2 diabetes is primarily attributed to increased apoptosis of pancreatic β-Cells. The aim of the present study was to investigate the effects of Schisandrae chinensis oil on pancreatic β-Cells in type 2 diabetes mellitus rats and the associated molecular mechanisms of action. Wistar rats were randomly divided into diabetic rats and control rats, diabetic rats treated with Schisandrae chinensis oil (1 mg/kg), and control rats treated with Schisandrae chinensis oil. The serum fasting blood glucose, insulin, total cholesterol, and triglyceride levels along with MDA content, SOD and CAT activities in pancreatic tissues were measured. TUNEL was used to observe the apoptosis of rat pancreatic cells. Western blot was used to determine specific protein expression. The results showed that the oil significantly decreased fasting blood glucose, total cholesterol, triglyceride levels as well as the pancreatic MDA, but increased SOD and CAT activities. The protein expression of Bcl-2, PDX-1, GLUT-2, and GCK but not caspase 3 was significantly enhanced in the oil-treated rats compared with diabetic rats. However, Bax content was not significantly different between the control and DM groups. Schisandra chinensis oil improves pancreatic β-cell function by enhancing antioxidant potential of the pancreas, upregulating the expression of anti-apoptotic genes, increasing expression of glucose metabolism, and delaying islet cell apoptosis.
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