Spondias purpurea L. (Anacardiaceae): Antioxidant and Antiulcer Activities of the Leaf Hexane Extract

Abstract

Spondias purpurea is used in folk medicine to treat diarrhea and diuresis. The objective of this study was to evaluate the phytochemical profile and antioxidant and antiulcer activities of the hexane extract of the leaves of S. purpurea (SpHE). Phytochemical profile was evaluated via thin layer chromatography (TLC) and HPLC. SpHE was screened for antioxidant activities using DPPH, ABTS, FRAP, and phosphomolybdenum assays. To determine its antiulcer properties, animals were pretreated with injured control, lansoprazole, ranitidine, carbenoxolone, or SpHE (12.5, 25, and 50 mg/kg) and were screened; acute ulcers were induced by HCl/ethanol, absolute ethanol, and nonsteroidal anti-inflammatory drug (NSAID). TLC revealed the presence of flavonoids, whereas HPLC analysis showed the presence of caffeic acid and epigallocatechin. The phenolic compounds and in vitro assays showed antioxidant activity. After gastric ulcer induction by using HCl/ethanol, SpHE reduced the area of ulcerative lesions by 82, 91, and 88%, respectively. In ethanol, SpHE reduced the area of ulcerative lesions by 77, 93, and 92%, respectively. In the NSAID, the percentages of protection were 70, 76, and 78%, respectively. SpHE promoted the minimization of ulcers, increased the levels of reduced glutathione, and decreased tumor necrosis factor. S. purpurea has antioxidant and antiulcer properties.

Figure 1

HPLC chromatograms of the hexane extract from leaves of Spondias purpurea. A, caffeic acid (26 min); B, epigallocatechin (32.25 min).

Figure 2

Effect of oral administration of SpHE on gastric lesions induced by HCl/ethanol in Swiss mice. Animals were treated orally with 1% Tween 80 aqueous solution (injured control (CL)), lansoprazole (30 mg/kg), and SpHE (12.5, 25, and 50 mg/kg). ULI: ulcerative lesion index. Results are expressed as mean ± SD (n = 5–6). ANOVA followed by Tukey's test, ^∗∗∗p < 0.001 when compared with CL.

Figure 3

Effect of different doses of SpHE on the severity of gastric lesion (gross examination) examined in HCl-/ethanol-induced gastric ulceration model. These photographs are typical of such tissues.

Figure 4

Effect of SpHE on gastric lesions induced by absolute ethanol in Wistar rats. Animals were treated orally with 1% Tween 80 aqueous solution (injured control (CL)), lansoprazole (30 mg/kg), and SpHE (12.5, 25, and 50 mg/kg). Ulcerative lesion area. Values represent the mean ± SD (n = 6). ANOVA followed by Tukey's test, ^∗∗∗p < 0.001 when compared with CL.

Figure 5

Effect of different doses of SpHE on the severity of gastric lesion (gross examination) examined in ethanol-induced gastric ulceration model. These photographs are typical of such tissues.

Figure 6

Effect of SpHE on gastric lesions induced by NSAID in Wistar rats. Animals were treated orally with 1% Tween 80 aqueous solution (injured control (CL)), ranitidine (60 mg/kg), and SpHE (12.5, 25, and 50 mg/kg). Ulcerative lesion area. Values represent the mean ± SD (n = 6). ANOVA followed by Tukey's test, ^∗∗∗p < 0.001 when compared with CL.

Figure 7

Effect of different doses of SpHE on the severity of gastric lesion (gross examination) examined in NSAID-induced gastric ulceration model. These photographs are typical of such tissues.

Figure 8

Histological analysis of the gastric mucosa of animals submitted to the induction of ulcer with HCl/ethanol. Animals were pretreated with 1% Tween 80 aqueous solution: injured control (a), lansoprazole (b), and SpHE 12.5 mg/kg (c), 25 mg/kg (d), and 50 mg/kg (e). Observed in (a): evidence of disorganization of the columnar simple epithelium in the gastric pits (enlarged detail, arrowhead) and gastric glands (arrows), congestion of the blood capillaries (enlarged detail, asterisk), and necrosis of the gastric mucosa cells (enlarged detail); in (b): preserved columnar simple epithelium in the gastric pits (enlarged detail) and well-preserved gastric glands (arrow); in (c): nonpreserved gastric mucosa with exfoliation of the simple columnar epithelium (enlarged detail); in (d): gastric mucosa with slight focal exfoliations of the simple columnar epithelium and preserved gastric mucosa (asterisk); and in (e): preserved gastric mucosa and simple columnar epithelium (enlarged detail).

Figure 9

Histological analysis of the gastric mucosa of animals submitted to the induction of ulcer with ethanol. Animals were pretreated with 1% Tween 80 aqueous solution: injured control (a), lansoprazole (b), and SpHE 12.5 mg/kg (c), 25 mg/kg (d), and 50 mg/kg (e). Observed in (a): disorganization of the columnar simple epithelium in the gastric pits (enlarged detail, arrowhead) and gastric glands (arrows), congestion of the blood capillaries (enlarged detail, asterisk), and necrosis of the gastric mucosa cells (arrowhead); in (b): columnar simple epithelium in the gastric pits (enlarged detail) and well-preserved gastric glands (arrows); in (c): poorly preserved gastric mucosa, exfoliations of the columnar simple epithelium, and necrosis of the superficial epithelium (enlarged detail); and in (d) and (e): well-preserved gastric mucosa (enlarged detail).

Figure 10

Histological analysis of the gastric mucosa of animals submitted to the induction of ulcer with NSAID (indomethacin). Animals were pretreated with 1% Tween 80 aqueous solution: injured control (a), ranitidine (b), and SpHE 12.5 mg/kg (c), 25 mg/kg (d), and 50 mg/kg (e). Observed in (a): disorganization of the gastric glands (arrows) and of the columnar simple epithelium in the gastric pits (enlarged detail, arrowhead) with cellular necrosis (dashed arrow); in (b): columnar simple epithelium of the pits (enlarged detail) and well-preserved gastric glands (arrows); in (c): gastric mucosa with slight exfoliations of the columnar simple epithelium and unpreserved gastric mucosa (asterisk); in (d): preserved gastric mucosa (asterisk) with exfoliations of discrete columnar epithelium (enlarged detail, arrow); and in (e): preserved gastric mucosa (asterisk) and simple columnar simple epithelium (enlarged detail).

Figure 11

Effect of oral administration of SpHE on nonprotein sulfhydryl group (GSH) concentrations in the gastric mucosa of the animals submitted to models of induction of acute ulcers by HCl/ethanol (a), ethanol (b), and NSAID (c). The experimental groups received 1% Tween 80 aqueous solution (injured control (CL)). Results are expressed as mean ± SD (n = 5). ANOVA followed by Tukey's test, ^∗∗∗p < 0.001 when compared with CL; ^##p < 0.01; ^###p < 0.001 when compared with noninjured control group (CN).

Figure 12

Effect of oral administration of SpHE on tumor necrosis factor alpha (TNF-α) concentrations in the gastric mucosa of the animals submitted to models of induction of acute ulcers by HCl/ethanol (a), ethanol (b), and NSAID (c). The experimental groups received 1% Tween 80 aqueous solution (injured control (CL)). Results are expressed as mean ± SD (n = 5). ANOVA followed by Tukey's test, ^∗∗p < 0.01; ^∗∗∗p < 0.001 when compared with CL; ^###p < 0.001 when compared with noninjured control group (CN).

Figure 13

Effect of oral administration of SpHE on nitric oxide (NO) concentrations in the gastric mucosa of the animals submitted to models of induction of acute ulcers by HCl/ethanol (a), ethanol (b), and NSAID (c). The experimental groups received 1% Tween 80 aqueous solution (injured control (CL)). Results are expressed as mean ± SD (n = 5). ANOVA followed by Tukey's test, ^∗∗∗p < 0.001 when compared with CL; ^###p < 0.001 when compared with noninjured control group (CN).