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Status of inflammatory markers and growth factor in gastric ulcer protective effects of Punica granatum L. peel extract in rat

Indal Chauhan, Sudhanshu Agrawal, Raj Kumar Goel.




Abstract
Cited by 24 Articles

Background: Inflammatory markers, namely, myeloperoxidase (MPO), cytokines (tumor necrosis factor-alpha [TNF-α], and interleukin-1 beta [IL-1β]) and vascular endothelial growth factor (VEGF) have been reported to play an important role in ulcerogenesis and healing. Recently, we reported that the gastric ulcer (GU) protective and healing effects of 50% ethanol (EtOH) extract of Punica granatum peel (PGE) in rats were predominantly due to strengthening of mucosal defense and antioxidants status.

Aims and Objectives: The present study incorporates the effects of PGE on rat gastric mucosal inflammatory markers (MPO, TNF-α, and IL-1β) and angiogenic factor (VEGF) in GU induced by cold-restraint stress (CRS) and EtOH in rats.

Materials and Methods: PGE (100 mg/kg) was administered orally once daily to rats for 7 days before induction of CRS and EtOH GU. Ulcer index (UI), gastric mucosal MPO, TNF-α, and IL-1β, and VEGF were estimated.

Results: CRS rats showed increase in UI and MPO (419.5, P < 0.001) compared with unstressed rats while PGE caused decrease in UI (46.1%, P < 0.05) and MPO (51.1%, P < 0.001) compared with CRS rats. EtOH rats showed increase in UI, TNF-α (936.5%, P < 0.001), IL-1β (37.2%, P < 0.05), and VEGF (13.0%, P < 0.05) compared with control normal saline-treated rats. PGE-treated EtOH rats showed decrease in UI (68.9%, P < 0.05), TNF-α (77.9%, P < 0.01), and IL-1β (24.8%, P < 0.05) but tended to decrease VEGF (7.3%, P < 0.2) compared with EtOH rats.

Conclusion: Both the inflammatory markers and VEGF were found to increase in GU rats while PGE EtOH extract decreased the status of inflammatory markers with little change in VEGF level with concomitant decrease in ulceration indicating their role in ulcer healing and repair.

Key words: Punica granatum Peel; Gastric Ulcer Healing; Myeloperoxidase; Tumor Necrosis Factor-alpha; Interleukin-1 Beta; Vascular Endothelial Growth Factor






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