MARATTO

article · Slovenian Veterinary Research

GREEN TEA MITIGATES STREPTOZOTOCIN-INDUCED DIABETIC MICE THROUGH ANTI-FIBROTIC ACTIVITY AND MODULATION OF PROINFLAMMATORY CYTOKINES

Abstract

This research was planned to assess the protective effect of green tea extract (GTE) in STZ-induced diabetes in mice. Seventy-five female albino mice were used. Mice randomly allocated into five groups of 15 mice in each as follows: group 1 (control), group 2 (STZ, diabetic), group 3 (green tea + STZ), group 4 (protective group with green tea), and group 5 (green tea only). Oral administration of the green tea extract for three weeks to diabetic mice resulted in significant regaining in body weight, decreased blood glucose, cholesterol, triglyceride, free fatty acid and low-density lipoprotein cholesterol (LDL-C) levels and lowered malondialdehyde (MDA) contents and increased total protein and high-density lipoprotein cholesterol (HDL-C) as compared to untreated diabetic group. Histopathological changes were compatible with these biochemical findings. Diabetic mice pre- or co-treated with green tea also exhibited a significant downregulation in TGFβ1 and TNFα genes expression. Green tea extracts had protective and antidiabetic effect in controlling blood glucose level in addition to improving lipid metabolism and body weight in diabetic mice.Key words: diabetes; green tea; liver; TNFα; TGF-Β1; mice

Research topics

  • Tea Polyphenols and Effects
  • Atherosclerosis and Cardiovascular Diseases

Read the original research

This page summarises published work. The authoritative version sits with the publisher.

DOI: 10.26873/svr-754-2019

Is something wrong with this record? Report it or request removal.

Discussion

Discuss this research

Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.

No discussion yet. Open the first thread.