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Gastroprotective Activities of Sennoside A and Sennoside B via the Up-Regulation of Prostaglandin E2 and the Inhibition of H(+)/K(+)-ATPase.

Hwang IY, Jeong CS - Biomol Ther (Seoul) (2015)

Bottom Line: It was observed that both sennoside A and sennoside B increased prostaglandin E2 (PGE2) levels and inhibited H(+)/K(+)-ATPase (proton pump).Furthermore, sennoside A and B increased PGE2 in a concentration-dependent manner.Our results thus suggest that sennoside A and sennoside B possess significant gastroprotective activities and they might be useful for the treatment of gastric disease.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Duksung Women's University, Seoul 132-714, Republic of Korea.

ABSTRACT
Sennoside A (erythro) and sennoside B (threo) are dianthrone glycosides and diastereomers. We investigated their abilities to prevent the gastric lesions associated with diseases, such as, gastritis and gastric ulcer. To elucidate their gastroprotective effects, the inhibitions of HCl•EtOH-induced gastritis and indomethacin-induced gastric ulcers were assessed in rats. It was observed that both sennoside A and sennoside B increased prostaglandin E2 (PGE2) levels and inhibited H(+)/K(+)-ATPase (proton pump). In a rat model, both compounds reduced gastric juice, total acidity and increased pH, indicating that proton pump inhibition reduces gastric acid secretion. Furthermore, sennoside A and B increased PGE2 in a concentration-dependent manner. In a gastric emptying and intestinal transporting rate experiment, both sennoside A and sennoside B accelerated motility. Our results thus suggest that sennoside A and sennoside B possess significant gastroprotective activities and they might be useful for the treatment of gastric disease.

No MeSH data available.


Related in: MedlinePlus

Quantitation of sennoside A and B on PGE2. The values are mean ± S.E.M. of 3 experiments. Significant difference *p<0.05; **p<0.01; ***p<0.001 compared to the control group.
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f4-bt-23-458: Quantitation of sennoside A and B on PGE2. The values are mean ± S.E.M. of 3 experiments. Significant difference *p<0.05; **p<0.01; ***p<0.001 compared to the control group.

Mentions: Quantitative analysis of PGE2 was performed using AGS gastric cells treated with or without sennoside A or B (Fig. 4). Sennoside A significantly increased concentration of PGE2 to 123.1 pg/mL and 151.4 pg/mL at doses of 50 μM and 100 μM, respectively. Similarly sennoside B increased concentration of PGE2 to 105.4 pg/mL and 173.6 pg/mL at doses of 50 μM and 100 μM, respectively. One of the gastric mucosal protectors, rebamipide, increased PGE2 levels to 185.1 pg/mL (50 μM) and 447.1 pg/mL (100 μM), whereas indomethacin, which inhibits the synthesis of PGE2 from arachidonic acid, decreased PGE2 levels to 29.6 pg/mL (50 μM) and 14.3 pg/mL (100 μM). These re sults show that sennoside A and B increase concentration of PGE2 in a dose-dependent manner, which implies that sennoside A and B have effective protective effects against gastric lesions.


Gastroprotective Activities of Sennoside A and Sennoside B via the Up-Regulation of Prostaglandin E2 and the Inhibition of H(+)/K(+)-ATPase.

Hwang IY, Jeong CS - Biomol Ther (Seoul) (2015)

Quantitation of sennoside A and B on PGE2. The values are mean ± S.E.M. of 3 experiments. Significant difference *p<0.05; **p<0.01; ***p<0.001 compared to the control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556206&req=5

f4-bt-23-458: Quantitation of sennoside A and B on PGE2. The values are mean ± S.E.M. of 3 experiments. Significant difference *p<0.05; **p<0.01; ***p<0.001 compared to the control group.
Mentions: Quantitative analysis of PGE2 was performed using AGS gastric cells treated with or without sennoside A or B (Fig. 4). Sennoside A significantly increased concentration of PGE2 to 123.1 pg/mL and 151.4 pg/mL at doses of 50 μM and 100 μM, respectively. Similarly sennoside B increased concentration of PGE2 to 105.4 pg/mL and 173.6 pg/mL at doses of 50 μM and 100 μM, respectively. One of the gastric mucosal protectors, rebamipide, increased PGE2 levels to 185.1 pg/mL (50 μM) and 447.1 pg/mL (100 μM), whereas indomethacin, which inhibits the synthesis of PGE2 from arachidonic acid, decreased PGE2 levels to 29.6 pg/mL (50 μM) and 14.3 pg/mL (100 μM). These re sults show that sennoside A and B increase concentration of PGE2 in a dose-dependent manner, which implies that sennoside A and B have effective protective effects against gastric lesions.

Bottom Line: It was observed that both sennoside A and sennoside B increased prostaglandin E2 (PGE2) levels and inhibited H(+)/K(+)-ATPase (proton pump).Furthermore, sennoside A and B increased PGE2 in a concentration-dependent manner.Our results thus suggest that sennoside A and sennoside B possess significant gastroprotective activities and they might be useful for the treatment of gastric disease.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Duksung Women's University, Seoul 132-714, Republic of Korea.

ABSTRACT
Sennoside A (erythro) and sennoside B (threo) are dianthrone glycosides and diastereomers. We investigated their abilities to prevent the gastric lesions associated with diseases, such as, gastritis and gastric ulcer. To elucidate their gastroprotective effects, the inhibitions of HCl•EtOH-induced gastritis and indomethacin-induced gastric ulcers were assessed in rats. It was observed that both sennoside A and sennoside B increased prostaglandin E2 (PGE2) levels and inhibited H(+)/K(+)-ATPase (proton pump). In a rat model, both compounds reduced gastric juice, total acidity and increased pH, indicating that proton pump inhibition reduces gastric acid secretion. Furthermore, sennoside A and B increased PGE2 in a concentration-dependent manner. In a gastric emptying and intestinal transporting rate experiment, both sennoside A and sennoside B accelerated motility. Our results thus suggest that sennoside A and sennoside B possess significant gastroprotective activities and they might be useful for the treatment of gastric disease.

No MeSH data available.


Related in: MedlinePlus