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Gastroprotective Mechanisms of the Monoterpene 1,8-Cineole (Eucalyptol).

Rocha Caldas GF, Oliveira AR, Araújo AV, Lafayette SS, Albuquerque GS, Silva-Neto Jda C, Costa-Silva JH, Ferreira F, Costa JG, Wanderley AG - PLoS ONE (2015)

Bottom Line: CIN (100 mg/kg) reduced the volume of basal but not stimulated acid secretion.This findings demonstrate the role of 1,8-cineole as an important ulcer healing agent and indicate the involvement of antioxidant and cytoprotective mechanisms in the gastroprotective effect of compound.This study also provides evidence that 1,8-cineole is related to the gastroprotective effect of the essential oil of Hyptis martiusii.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Sciences, Universidade Federal de Pernambuco, 50740-521, Recife, PE, Brazil.

ABSTRACT
Recently, our research group identified and reported 1,8-cineole (CIN), a monoterpene that naturally occur in many aromatic plants, as one of the major constituent of the essential oil from leaves of Hyptis martiusii (EOHM), as well as characterized the gastroprotective action of this oil. The aim of this study was to investigate the mechanisms of action involved in the antiulcer and healing activity of CIN, in order to confirm its correlation with the gastroprotective effect of EOHM. Wistar rats were exposed to different protocols (acute ulceration, gastrointestinal motility and antisecretory activity). In addition, were determinated the involvement of nitric oxide and sulphydryl groups; the levels of gastric mucus, lipid peroxidation, sulphydryl groups and myeloperoxidase activity. The healing ability was evaluated by acetic acid-induced chronic ulcer and histological and immunohistochemical analysis (PCNA, Ki-67 and BrdU). The treatment with CIN inhibited ethanol-, ethanol/HCl- and indomethacin-induced gastric lesions. The highest doses of CIN inhibited gastric emptying, but did not affect intestinal transit. CIN (100 mg/kg) reduced the volume of basal but not stimulated acid secretion. CIN increased levels of mucus (89.3%), prevented depletion of -SH groups (62.6%) and reduced the level of lipid peroxidation (55.3%) and myeloperoxidase activity (59.4%) in the gastric mucosa. In chronic ulcer model, CIN reduced in 43.1% the gastric area lesion, promoted significant regeneration and restoration of the levels of mucus in glandular cells as confirmed by histological analysis; and promoted increase in cell proliferation as evidenced by reactivity for PCNA, Ki-67 and BrdU. This findings demonstrate the role of 1,8-cineole as an important ulcer healing agent and indicate the involvement of antioxidant and cytoprotective mechanisms in the gastroprotective effect of compound. This study also provides evidence that 1,8-cineole is related to the gastroprotective effect of the essential oil of Hyptis martiusii.

No MeSH data available.


Related in: MedlinePlus

Effect of 1,8-cineole (CIN) on healing of the gastric mucosa in the rats subjected to induction of chronic ulcer by 30% acetic acid.Animals were treated orally with 1% Tween-80 aqueous solution (control group), pantoprazole (P, 40 mg/kg) or CIN (100 mg/kg) for 14 days. (A) Lesion area, (B) body weight during treatment and (C) macroscopical appearance of the gastric ulcer. Values represent the mean ± S. E. M. for 6 animals. *Statistically different from control group, ANOVA followed by Tukey's test (*p < 0.05 vs. control group).
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pone.0134558.g002: Effect of 1,8-cineole (CIN) on healing of the gastric mucosa in the rats subjected to induction of chronic ulcer by 30% acetic acid.Animals were treated orally with 1% Tween-80 aqueous solution (control group), pantoprazole (P, 40 mg/kg) or CIN (100 mg/kg) for 14 days. (A) Lesion area, (B) body weight during treatment and (C) macroscopical appearance of the gastric ulcer. Values represent the mean ± S. E. M. for 6 animals. *Statistically different from control group, ANOVA followed by Tukey's test (*p < 0.05 vs. control group).

Mentions: In the acetic acid model, the results show that oral administration of CIN (100 mg/kg) for 14 consecutive days decreased (43.1%) the area of chronic ulcer to 27.3 ± 3.2 mm2 as can be seen in Fig 2A. Pantoprazole (40 mg/kg) speeded up the healing of gastric ulcer, significantly reducing the area of the injury to 20.1 ± 6.2 mm2 (58.1%), when compared to the control group (48.0 ± 7.5 mm2). During the 14 days of treatment, CIN or pantoprazole did not produce any visible signs of toxicity. The animals treated with CIN showed a profile of body weight gain similar to animals of control group. (Fig 2B). The macroscopic appearance of the chronic ulcer induced by acetic acid in the gastric mucosa in control and in the pantoprazole or CIN- treated groups is represented in Fig 2C.


Gastroprotective Mechanisms of the Monoterpene 1,8-Cineole (Eucalyptol).

Rocha Caldas GF, Oliveira AR, Araújo AV, Lafayette SS, Albuquerque GS, Silva-Neto Jda C, Costa-Silva JH, Ferreira F, Costa JG, Wanderley AG - PLoS ONE (2015)

Effect of 1,8-cineole (CIN) on healing of the gastric mucosa in the rats subjected to induction of chronic ulcer by 30% acetic acid.Animals were treated orally with 1% Tween-80 aqueous solution (control group), pantoprazole (P, 40 mg/kg) or CIN (100 mg/kg) for 14 days. (A) Lesion area, (B) body weight during treatment and (C) macroscopical appearance of the gastric ulcer. Values represent the mean ± S. E. M. for 6 animals. *Statistically different from control group, ANOVA followed by Tukey's test (*p < 0.05 vs. control group).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4526535&req=5

pone.0134558.g002: Effect of 1,8-cineole (CIN) on healing of the gastric mucosa in the rats subjected to induction of chronic ulcer by 30% acetic acid.Animals were treated orally with 1% Tween-80 aqueous solution (control group), pantoprazole (P, 40 mg/kg) or CIN (100 mg/kg) for 14 days. (A) Lesion area, (B) body weight during treatment and (C) macroscopical appearance of the gastric ulcer. Values represent the mean ± S. E. M. for 6 animals. *Statistically different from control group, ANOVA followed by Tukey's test (*p < 0.05 vs. control group).
Mentions: In the acetic acid model, the results show that oral administration of CIN (100 mg/kg) for 14 consecutive days decreased (43.1%) the area of chronic ulcer to 27.3 ± 3.2 mm2 as can be seen in Fig 2A. Pantoprazole (40 mg/kg) speeded up the healing of gastric ulcer, significantly reducing the area of the injury to 20.1 ± 6.2 mm2 (58.1%), when compared to the control group (48.0 ± 7.5 mm2). During the 14 days of treatment, CIN or pantoprazole did not produce any visible signs of toxicity. The animals treated with CIN showed a profile of body weight gain similar to animals of control group. (Fig 2B). The macroscopic appearance of the chronic ulcer induced by acetic acid in the gastric mucosa in control and in the pantoprazole or CIN- treated groups is represented in Fig 2C.

Bottom Line: CIN (100 mg/kg) reduced the volume of basal but not stimulated acid secretion.This findings demonstrate the role of 1,8-cineole as an important ulcer healing agent and indicate the involvement of antioxidant and cytoprotective mechanisms in the gastroprotective effect of compound.This study also provides evidence that 1,8-cineole is related to the gastroprotective effect of the essential oil of Hyptis martiusii.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical Sciences, Universidade Federal de Pernambuco, 50740-521, Recife, PE, Brazil.

ABSTRACT
Recently, our research group identified and reported 1,8-cineole (CIN), a monoterpene that naturally occur in many aromatic plants, as one of the major constituent of the essential oil from leaves of Hyptis martiusii (EOHM), as well as characterized the gastroprotective action of this oil. The aim of this study was to investigate the mechanisms of action involved in the antiulcer and healing activity of CIN, in order to confirm its correlation with the gastroprotective effect of EOHM. Wistar rats were exposed to different protocols (acute ulceration, gastrointestinal motility and antisecretory activity). In addition, were determinated the involvement of nitric oxide and sulphydryl groups; the levels of gastric mucus, lipid peroxidation, sulphydryl groups and myeloperoxidase activity. The healing ability was evaluated by acetic acid-induced chronic ulcer and histological and immunohistochemical analysis (PCNA, Ki-67 and BrdU). The treatment with CIN inhibited ethanol-, ethanol/HCl- and indomethacin-induced gastric lesions. The highest doses of CIN inhibited gastric emptying, but did not affect intestinal transit. CIN (100 mg/kg) reduced the volume of basal but not stimulated acid secretion. CIN increased levels of mucus (89.3%), prevented depletion of -SH groups (62.6%) and reduced the level of lipid peroxidation (55.3%) and myeloperoxidase activity (59.4%) in the gastric mucosa. In chronic ulcer model, CIN reduced in 43.1% the gastric area lesion, promoted significant regeneration and restoration of the levels of mucus in glandular cells as confirmed by histological analysis; and promoted increase in cell proliferation as evidenced by reactivity for PCNA, Ki-67 and BrdU. This findings demonstrate the role of 1,8-cineole as an important ulcer healing agent and indicate the involvement of antioxidant and cytoprotective mechanisms in the gastroprotective effect of compound. This study also provides evidence that 1,8-cineole is related to the gastroprotective effect of the essential oil of Hyptis martiusii.

No MeSH data available.


Related in: MedlinePlus