Brief Article
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World J Gastroenterol. Feb 28, 2014; 20(8): 2085-2090
Published online Feb 28, 2014. doi: 10.3748/wjg.v20.i8.2085
Protective effects of D-002 on experimentally induced gastroesophageal reflux in rats
Zullyt Zamora, Vivian Molina, Rosa Mas, Yazmin Ravelo, Yohany Perez, Ambar Oyarzabal
Zullyt Zamora, Vivian Molina, Rosa Mas, Yazmin Ravelo, Yohany Perez, Ambar Oyarzabal, Department of Pharmacology, Centre of Natural Products, National Centre for Scientific Research, Havana 10600, Cuba
Author contributions: Zamora Z and Molina V prepared the draft study design, performed the experiments, analyzed the data, and wrote the first version of the manuscript; Mas R provided the original concept of the study, reviewed critically the study design and data analysis, and wrote further versions of the manuscript; Ravelo Y participated in conducting the experiments, data acquisition and analysis, and reviewed the manuscript; Perez Y and Oyarzabal A conducted the biochemical tests and reviewed aspects concerning oxidative variables; all the authors gave final approval of the version of the manuscript to be published.
Correspondence to: Zullyt Zamora, PhD, Department of Pharmacology, Centre of Natural Products, National Centre for Scientific Research, PO Box 6880, Cubanacan, Havana 10600, Cuba. zullyt.zamora@cnic.edu.cu
Telephone: +53-7-2714200 Fax: +53-7-336837
Received: July 7, 2013
Revised: August 26, 2013
Accepted: December 12, 2013
Published online: February 28, 2014
Processing time: 234 Days and 8.2 Hours
Abstract

AIM: To investigate the effects of beeswax alcohols (D-002) on the esophageal damage induced by gastroesophageal reflux (GER) in rats.

METHODS: Sixty male rats were randomized into six groups (10 rats/group): a negative control and five groups with experimentally induced GER: a positive vehicle control, three treated with D-002 (25, 100 and 200 mg/kg, respectively), and one with omeprazole 10 mg/kg. All treatments were given by gastric gavage. One hour after dosing, GER was produced by simultaneous ligation of the pyloric end and the forestomach. Esophageal lesions index (ELI), gastric secretion volume and acidity, and esophageal malondialdehyde (MDA) and sulfhydryl (SH) group concentrations were measured. Statistical significance was considered at P < 0.05.

RESULTS: As compared to the negative control, the positive control group exhibited increased ELI (5.2 ± 0.33 vs 0 ± 0, P = 0.0003), gastric secretion volume (2.69 ± 0.09 vs 0.1 ± 0.0, P = 0.0003) and acidity (238 ± 19.37 vs 120.0 ± 5.77, P = 0.001), and esophageal concentrations of MDA (2.56 ± 0.1 vs 1.76 ± 0.28, P = 0.001) and SH groups (1.02 ± 0.05 vs 0.56 ± 0.08, P = 0.0003). D-002 (25, 100 and 200 mg/kg) reduced ELI (3.36 ± 0.31, 2.90 ± 0.46 and 2.8 ± 0.23, respectively) vs the positive control (5.2 ± 0.33) (P = 0.004; P = 0.002; P = 0.001, respectively). There were no significant changes in acidity with D-002 treatment, and only the highest dose reduced the volume of the gastric secretion (1.92 ± 0.25) vs the positive control (2.69 ± 0.09, P = 0.013). D-002 (25, 100 and 200 mg/kg) lowered the esophageal MDA (2.05 ± 0.16, 1.98 ± 0.22 and 1.93 ± 0.22, respectively) (P = 0.01; P = 0.03; P = 0.03, respectively) and SH group concentration (0.87 ± 0.06, 0.79 ± 0.08 and 0.77 ± 0.06, respectively) (P = 0.04; P = 0.04; P = 0.02) vs the positive control (2.56 ± 0.10 and 1.02 ± 0.05, respectively). Omeprazole decreased ELI (2.54 ± 0.47), gastric secretion volume (1.97 ± 0.14) and acidity (158.5 ± 22.79), esophageal MDA (1.87 ± 0.13) and SH group (0.72 ± 0.05) concentrations vs the positive control (P = 0.002; P = 0.001; P = 0.02; P = 0.003; P = 0.002, respectively).

CONCLUSION: Acute oral administration of D-002 decreased macroscopic esophageal lesions and oxidative stress in rats with experimentally induced GER, without modifying gastric secretion acidity.

Keywords: D-002; Beeswax alcohols; Esophagitis; Gastroesophageal reflux; Oxidative stress

Core tip: Beeswax alcohols (D-002) has gastroprotective effects in experimental and clinical studies. However, the effects of D-002 on gastroesophageal reflux (GER) have not been investigated. We demonstrated that acute oral administration of 25, 100 and 200 mg/kg D-002 decreased the esophageal lesion index, and esophageal malondialdehyde and sulfhydryl group concentrations. Only the highest dose of D-002 reduced the gastric secretion volume, but none modified the acidity. D-002 decreased esophageal lesions and esophageal concentrations of lipid peroxidation and protein oxidation markers in rats with experimental GER, without modifying gastric secretion acidity.