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. 2014 Feb 10:14:49.
doi: 10.1186/1472-6882-14-49.

Pretreatment of Gymnema sylvestre revealed the protection against acetic acid-induced ulcerative colitis in rats

Abdulaziz M Aleisa, Salim S Al-Rejaie  1 , Hatem M Abuohashish, Mohammed S Ola, Mihir Y Parmar, Mohammed M Ahmed
Affiliations

Pretreatment of Gymnema sylvestre revealed the protection against acetic acid-induced ulcerative colitis in rats

Abdulaziz M Aleisa et al. BMC Complement Altern Med. .

Abstract

Background: Overproduction of free radicals and decreased antioxidant capacity are well-known risk factors for inflammatory bowel diseases. Gymnema sylvestre (GS) leaves extract is distinguished for its anti-diabetic, antioxidant and anti-inflammatory properties. Present study is designed to evaluate the preventative activities of GS against acetic acid (AA)-induced ulcerative colitis in Wistar rats.

Methods: Experimentally ulcerative colitis (UC) was induced by AA in animals pretreated with three different doses of GS leaves extract (50, 100, 200 mg/kg/day) and a single dose of mesalazine (MES, 300 mg/kg/day) for seven days. Twenty four hours later, animals were sacrificed and the colonic tissues were collected. Colonic mucus content was determined using Alcian blue dye binding technique. Levels of thiobarbituric acid reactive substances (TBARS), total glutathione sulfhydryl group (T-GSH) and non-protein sulfhydryl group (NPSH) as well as the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were estimated in colon tissues. Colonic nucleic acids (DNA and RNA) and total protein (TP) concentrations were also determined. Levels of pro-inflammatory cytokines including interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) as well as prostaglandin E2 (PGE2) and nitric oxide (NO) were estimated in colonic tissues. The histopathological changes of the colonic tissues were also observed.

Results: In AA administered group TBARS levels were increased, while colonic mucus content, T-GSH and NP-SH, SOD and CAT were reduced in colon. Pretreatment with GS inhibited TBARS elevation as well as mucus content, T-GSH and NP-SH reduction. Enzymatic activities of SOD and CAT were brought back to their normal levels in GS pretreated group. A significant reduction in DNA, RNA and TP levels was seen following AA administration and this inhibition was significantly eliminated by GS treatment. GS pretreatment also inhibited AA-induced elevation of pro-inflammatory cytokines, PGE2 and NO levels in colon. The apparent UC protection was further confirmed by the histopathological screening.

Conclusion: The GS leaves extract showed significant amelioration of experimentally induced colitis, which may be attributed to its anti-inflammatory and antioxidant property.

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Figures

Figure 1
Figure 1
Effect of GS (Gs) on [A] colon weight/length and [B] mucus content of rats in AA-induced UC. Data are expressed as mean ± SEM (n = 6) and analyzed using one-way ANOVA followed by Student-Newman-Keuls multiple comparisons test. The statistical significance was considered as *P < 0.05, **P < 0.01 and ***P < 0.001 where ‘a’ compared with control and ‘b’ compared with AA.
Figure 2
Figure 2
Effect of GS (Gs) on colonic level of [A] TBARS, [B] T-GSH and [C] NPSH of rats in AA induced UC. Data are expressed as mean ± SEM (n = 6) and analyzed using one-way ANOVA followed by Student-Newman-Keuls multiple comparisons test. The statistical significance was considered as *P < 0.05, **P < 0.01 and ***P < 0.001 where ‘a’ compared with control and ‘b’ compared with AA.
Figure 3
Figure 3
Effect of GS (Gs) on colonic activities of [A] SOD and [B] CAT of rats in AA induced UC. Data are expressed as mean ± SEM (n = 6) and analyzed using one-way ANOVA followed by Student-Newman-Keuls multiple comparisons test. The statistical significance was considered as *P < 0.05, **P < 0.01 and ***P < 0.001 where ‘a’ compared with control and ‘b’ compared with AA.
Figure 4
Figure 4
Effect of GS (Gs) on colonic conc of [A] DNA, [B] RNA and [C] TP of rats in AA induced UC. Data are expressed as mean ± SEM (n = 6) and analyzed using one-way ANOVA followed by Student-Newman-Keuls multiple comparisons test. The statistical significance was considered as *P < 0.05, **P < 0.01 and ***P < 0.001 where ‘a’ compared with control and ‘b’ compared with AA.
Figure 5
Figure 5
Effect of GS (Gs) on colonic level of [A] IL-1β, [B] TNF-α and [C] IL-6 of rats in AA induced UC. Data are expressed as mean ± SEM (n = 6) and analyzed using one-way ANOVA followed by Student-Newman-Keuls multiple comparisons test. The statistical significance was considered as *P < 0.05, **P < 0.01 and ***P < 0.001 where ‘a’ compared with control and ‘b’ compared with AA.
Figure 6
Figure 6
Effect of GS (Gs) on colonic level of [A] PGE2 and [B] NO of rats in AA induced UC. Data are expressed as mean ± SEM (n = 6) and analyzed using one-way ANOVA followed by Student-Newman-Keuls multiple comparisons test. The statistical significance was considered as *P < 0.05, **P < 0.01 and ***P < 0.001 where ‘a’ compared with control and ‘b’ compared with AA.
Figure 7
Figure 7
Histopathological sections of colons from rats stained with H&E (400X). Colonic microscopic image of [A] Normal rat colon from Cont group with intact mucosal layer and epithelial; [B] AA treated rat colon with diffused active colitis, extensive damage including edema in submucosa and chronic inflammatory cells infiltrate with widely ulcerating mucosa, and hemorrhages; [C, D & E] dose dependent reparative epithelial changes and ulcer healing with lymphoid follicle in colon of GS treated rats (50, 100 and 200 mg/kg , respectively); [F] attenuated cell damage with complete ulcer healing in MES treated group.
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References

    1. Sood A, Midha V, Sood N, Bhatia AS, Avasthi G. Incidence and prevalence of ulcerative colitis in Punjab. North India. Gut. 2003;52(11):1587–1590. - PMC - PubMed
    1. Olden KW. Diagnosis of irritable bowel syndrome. Gastroenterology. 2002;122(6):1701–1714. doi: 10.1053/gast.2002.33741. - DOI - PubMed
    1. Nieto N, Torres MI, Rios A, Gil A. Dietary polyunsaturated fatty acids improve histological and biochemical alterations in rats with experimental ulcerative colitis. J Nutr. 2002;132(1):11–19. - PubMed
    1. Slamon ND, Pentreath VW. Antioxidant defense against antidepressants in C6 and 1321 N1 cells. Chem Biol Interact. 2000;127(3):181–199. doi: 10.1016/S0009-2797(00)00172-1. - DOI - PubMed
    1. Cetinkaya A, Bulbuloglu E, Kantarceken B, Ciralik H, Kurutas EB, Buyukbese MA, Gumusalan Y. Effects of L-carnitine on oxidant/antioxidant status in acetic acid-induced colitis. Dig Dis Sci. 2006;51(3):488–494. doi: 10.1007/s10620-006-3160-9. - DOI - PubMed

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