Article Publish Status: FREE
Abstract Title:

Protective and hypoglycemic effects of celery seed on streptozotocin-induced diabetic rats: experimental and histopathological evaluation.

Abstract Source:

Acta Diabetol. 2016 Mar 4. Epub 2016 Mar 4. PMID: 26940333

Abstract Author(s):

Faezeh Tashakori-Sabzevar, Masoud Ramezani, Hossein Hosseinzadeh, Seyyed Mohammad Reza Parizadeh, Ahmad Reza Movassaghi, Ahmad Ghorbani, Seyed Ahmad Mohajeri

Article Affiliation:

Faezeh Tashakori-Sabzevar


AIMS: Diabetes mellitus is a major manifestation of metabolic disorder which presents with hyperglycemia (high levels of serum blood sugar). In the present study, we aimed to investigate the effects of celery seed extract on different biochemical factors and histopathological changes in normal and streptozotocin (STZ)-induced diabetic rats.

METHODS: A total of 35 male Wistar rats were divided into five groups (one normal and four diabetic groups). STZ was injected intraperitoneally to induce diabetes. The effects of hexane extract of celery seed and glibenclamide (as a positive control) were compared. Blood samples were analyzed on days 0, 18, and 33, and histopathological evaluations were performed at the end of the study.

RESULTS: Glucose, triglycerides, and cholesterol levels significantly decreased, whereas insulin and high-density lipoprotein (HDL) levels increased in the extract-administered groups, as compared to the negative diabetic control group (P < 0.0001). The concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum of the extract-administered groups were significantly less than the negative control group (P < 0.0001). Histopathological reports revealed significantly less atrophy, necrosis, and inflammation in the rats receiving celery seed extract compared to the negative control group.

CONCLUSIONS: The results indicated that celery seed extract can be effective in controlling hyperglycemia and hyperlipidemia in diabetic rats, and demonstrated its protective effects against pancreatic toxicity resulting from STZ-induction.

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