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. 2013 Jul 19:13:183.
doi: 10.1186/1472-6882-13-183.

Gastroprotective effect of desmosdumotin C isolated from Mitrella kentii against ethanol-induced gastric mucosal hemorrhage in rats: possible involvement of glutathione, heat-shock protein-70, sulfhydryl compounds, nitric oxide, and anti-Helicobacter pylori activity

Heyam Mohamed Ali Sidahmed, Ainnul Hamidah Syahadah Azizan, Syam Mohan, Mahmood Ameen Abdulla, Siddig Ibrahim Abdelwahab, Manal Mohamed Elhassan Taha, A Hamid A Hadi, Kamal Aziz Ketuly, Najihah Mohd Hashim, Mun Fai Loke, Jamuna Vadivelu

Gastroprotective effect of desmosdumotin C isolated from Mitrella kentii against ethanol-induced gastric mucosal hemorrhage in rats: possible involvement of glutathione, heat-shock protein-70, sulfhydryl compounds, nitric oxide, and anti-Helicobacter pylori activity

Heyam Mohamed Ali Sidahmed et al. BMC Complement Altern Med. .

Retraction in

Abstract

Background: Mitrella kentii (M. kentii) (Bl.) Miq, is a tree-climbing liana that belongs to the family Annonaceae. The plant is rich with isoquinoline alkaloids, terpenylated dihydrochalcones and benzoic acids and has been reported to possess anti-inflammatory activity. The purpose of this study is to assess the gastroprotective effects of desmosdumotin C (DES), a new isolated bioactive compound from M. kentii, on gastric ulcer models in rats.

Methods: DES was isolated from the bark of M. kentii. Experimental rats were orally pretreated with 5, 10 and 20 mg/kg of the isolated compound and were subsequently subjected to absolute ethanol-induced acute gastric ulcer. Gross evaluation, mucus content, gastric acidity and histological gastric lesions were assessed in vivo. The effects of DES on the anti-oxidant system, non-protein sulfhydryl (NP-SH) content, nitric oxide (NO)level, cyclooxygenase-2 (COX-2) enzyme activity, bcl-2-associated X (Bax) protein expression and Helicabacter pylori (H pylori) were also investigated.

Results: DES pre-treatment at the administered doses significantly attenuated ethanol-induced gastric ulcer; this was observed by decreased gastric ulcer area, reduced or absence of edema and leucocytes infiltration compared to the ulcer control group. It was found that DES maintained glutathione (GSH) level, decreased malondialdehyde (MDA) level, increased NP-SH content and NO level and inhibited COX-2 activity. The compound up regulated heat shock protein-70 (HSP-70) and down regulated Bax protein expression in the ulcerated tissue. DES showed interesting anti-H pylori effects. The efficacy of DES was accomplished safely without any signs of toxicity.

Conclusions: The current study reveals that DES demonstrated gastroprotective effects which could be attributed to its antioxidant effect, activation of HSP-70 protein, intervention with COX-2 inflammatory pathway and potent anti H pylori effect.

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Figures

Figure 1
Figure 1
Chemical structure of desmosdumotin C.
Figure 2
Figure 2
Gross evaluation. Macroscopic appearance of the gastric mucosa of the rats pre-treated with DES at doses 5, 10, 20 mg/kg (D,E, F) or omeprazole 20 mg/kg (C) showed reduced lesion formation when compared to the ulcer control rats (B) 2C. Ethanol-induced sever injuries to the gastric mucosa appear as elongated bands of haemorrhage (white arrow). (A) Showed normal macroscopic appearance of the intact stomach from normal group. (magnification: 1.8×).
Figure 3
Figure 3
Histological evaluation. The gastric mucosa of the rats pretreated with DES at doses 5, 10, 20 mg/kg (D, E, F) or omeprazole (C) showed improved histological appearance compared to ulcer control rats (B) which have extensive visible hemorrhagic necrosis of the gastric mucosa with edema and leucocytes infiltration of submucosa. The black arrow indicates edema in submucosa and the white arrow indicates disruption to the deep mucosa layer. (A) showed normal histological apperance of the intact stomach from normal group. (H & E stain: 20×).
Figure 4
Figure 4
Tissue glycoprotein. Effect of DES on gastric tissue glycoprotein-PAS staining in ethanol-induced gastric ulcer in rats where (A) normal group, (B) ulcer group, (C) omeprazole group, (D, E, F) treated DES groups at doses 5, 10 and 20 mg/kg, respectively, where the black arrows indicates the glycoprotein appear as magenta stain (PAS stain 20×).
Figure 5
Figure 5
Immunohistochemical analysis of Hsp-70 protein. HSP-70 expression in the gastric tissue of rats submitted to ethanol-induced gastric mucosal lesions at different groups where (A) normal control group, (B) ulcer control group (B), (C) omeprazole group, (D, E, F) the pre-treated groups with DES at doses 5, 10 and 20 mg/kg, respectively. The antigen site appears as a brown color (IHC: 20×).
Figure 6
Figure 6
Immunohistochemical analysis of Bax protein. Bax expression in the gastric tissue of rats submitted to ethanol-induced gastric mucosal lesions at different groups where (A) normal control group, (B) ulcer control group, (C) omeprazole group, (D, E, F) pre-treated group with DES at doses 5, 10 and 20 mg/kg, respectively. The antigen site appears as a brown color (IHC: 20×).
Figure 7
Figure 7
Effect of DES on gastric tissue homogenate content of (A) Glutathione (GSH), (B) Malondialdehyde (MDA), (C) Non protein sulfhydryl (NP-SH) and (D) Nitric oxide (NO). DES pre-treatment significantly increased GSH, decreased MDA and replenished NP-SH and NO content. Statistical analysis was assessed with ordinary one way ANOVA followed by Dunnett ’ s Multiple comparison tests. All values are represented as mean of 3 – 5 animals. ± SEM. * indicates (p < 0.05) compared to ulcer control. $ indicates (p < 0.05) statistical differences compared to omeprazole group.
Figure 8
Figure 8
Inhibition of COX-2 enzyme. DES was observed to inhibit COX-2 catalyzed prostaglandin biosynthesis by 29.5% and 34.8% at 250 and 500 ng/ml, respectively, compared with indomethacin as COX-2 inhibitor shows inhibition of 71.37%. The results represent as mean ± SEM.
Figure 9
Figure 9
Ferric reducing/antioxidant power assay. The FRAP value (μM Fe (II)/g dry mass) of DES in compare with that of ascorbic acid and gallic acid.
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