Gastroprotective effect of palmatine against acetic acid-induced gastric ulcers in rats
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Gastric ulcers are one of the most common gastrointestinal disorders. The aim of this study was to investigate the gastroprotective activity and possible underlying mechanisms of palmatine against acetic acid-induced gastric ulcers in rats. Palmatine was administered orally for 7 consecutive days to treat ulcers. The ulcer area, ulcer inhibition rate, histological section, platelet-activating factor (PAF) level in serum, prostaglandin E2 (PGE2) level in gastric tissue, 5-hydroxytryptamine (5-HT) level in the brain and norepinephrine (NE) level in the adrenal glands were analyzed. Histological results showed that the ulcer areas were significantly decreased by both doses of palmatine (10 and 20 mg/kg/day) compared with the model group, and the ulcer inhibition rates were 51.42% and 60.92%, respectively. Palmatine treatment markedly increased the level of PGE2 and decreased PAF, compared with the model group; however, it had no significant effect on 5-HT and NE levels. The results indicated that palmatine may exert a gastroprotective effect against gastric ulcers, and the mechanisms might be associated with the anti-inflammatory status and the protection of gastric mucosa via increasing PGE2 and decreasing PAF rather than neurohumoral regulation through 5-HT and NE. Thus, palmatine is a potential drug for treatment of gastric ulcers.
KeywordsPalmatine Gastroprotective action Acetic acid-induced gastric ulcer Anti-inflammation
Enzyme-linked immunosorbent assay
Low-dose palmatine group
High-dose palmatine group
Standard error of measurement
One-way analysis of variance
Prostaglandin E synthase
Hypothalamic pituitary adrenal
This work was supported by the National Natural Science Foundation of China (81573565), the College Students Innovation Project for the R&D of Novel Drugs (J1030830) and National Training Programs of Innovation and Entrepreneurship for College Students.
Compliances with ethical standards
Conflict of interest
We have no conflict of interest in this research.
- 8.Konturek SJ, Konturek PC, Brzozowski T (2005) Prostaglandins and ulcer healing. J Physiol Pharmacol 56(Suppl 5):5–31Google Scholar
- 13.Xian X, Sun B, Ye X, Zhang G, Hou P, Gao H (2014) Identification and analysis of alkaloids in cortex Phellodendron amurense by high-performance liquid chromatography with electrospray ionization mass spectrometry coupled with photodiode array detection. J Sep Sci 37:1533–1545CrossRefPubMedGoogle Scholar
- 26.Jimenez MP, Sainz SR (1997) The role of prostaglandins in the defense of the gastric mucosal barrier. Gastroenterol Hepatol 20(Suppl 2):16–21Google Scholar
- 32.Malison RT, Price LH, Berman R, van Dyck CH, Pelton GH, Carpenter L, Sanacora G, Owens MJ, Nemeroff CB, Rajeevan N, Baldwin RM, Seibyl JP, Innis RB, Charney DS (1998) Reduced brain serotonin transporter availability in major depression as measured by [123I]-2 beta-carbomethoxy-3 beta-(4-iodophenyl)tropane and single photon emission computed tomography. Biol Psychiatry 44:1090–1098CrossRefPubMedGoogle Scholar
- 34.Sanchez C, Bergqvist PB, Brennum LT, Gupta S, Hogg S, Larsen A, Wiborg O (2003) Escitalopram, the S-(+)-enantiomer of citalopram, is a selective serotonin reuptake inhibitor with potent effects in animal models predictive of antidepressant and anxiolytic activities. Psychopharmacology 167:353–362CrossRefPubMedGoogle Scholar