Abstract
This study was conducted to investigate the therapeutic effect of hydro-alcoholic extract of Spirulina platensis (SP), golden kiwifruit (Actinidia chinensis) flesh (KF), and golden kiwifruit peel (KP) individually or in combination (SFP) on indomethacin-induced gastric ulcer in rats. Negative control rats (GI) were orally administered distilled water in parallel with other treatments. The positive control rat group (GII) was administered 30 mg kg−1 indomethacin to induce gastric ulcers. The KF and KF extracts were used individually or together with SP in treating indomethacin-induced gastric ulcerated rat groups. Gastric ulcerated rat’s groups GIII, GIV, GV, GVI, and GVII were orally administered at 30 mg kg−1 rat body weight as total phenolic content (TPC) equivalent from SP, KF, KP, SPF extracts, and Lansoprazole (30 mg kg−1, as reference drug) daily up to 14 days, respectively. The relevant biochemical parameters, antioxidant biomarkers, and histopathological examination were examined. Remarkably, treating rats with SP, KF, KP, and SFP extracts markedly reduced gastric juice and stomach volume expansion induced by indomethacin. The SP significantly retrieved the pH of gastric juice to a regular rate compared to GI. The ulcer index (UI) was significantly attenuated by SP, KF, KP, and SFP administration. The protection index percentage (PI %) was 80.79, 54.51, 66.08, 75.74, and 74.86% in GIII, GIV, GV, GVI, and GVII, respectively. The gastric mucin content was significantly better attenuated by 95.7 in GIII compared to its content in GI. Lansoprazole increased mucin content by 80.3%, which was considerably lower than SP and SFP. SP, KF, KP, SFP, and Lansoprazole improved the reform of gastric mucosal-increased secreted mucus by 95.6, 61.3, 64.8, 103.1, and 80.2% in GIII, GIV, GV, GVI, and GVII, respectively. Interestingly, SFP efficiently increased vit. B12 level by 46.0% compared to other treatments. While Lansoprazole administrating did not significantly attenuate vit. B12 level. The SP and SFP improved iron and Hemoglobin (HB) levels depending on treatment. SP, KF, KP, and SFP significantly decreased the malondialdehyde (MDA) and increased reduced glutathione (GSH) as well as superoxide dismutase (SOD) levels in blood and stomach tissues. The most potent effect was observed with SP, and SFP was even better than Lansoprazole. Histopathologically, treating rats with SP extract showed a marked reduction of gastric damage and severity changes induced by indomethacin. KP was much better than KF in lessening gastric histopathological damages caused by indomethacin. SFP significantly alleviates gastric histopathological alterations. The lansoprazole-treated group (GVII) greatly relieved the gastric histopathological changes and recorded mild focal necrosis and desquamation of the mucosa in addition to mild oedema in the serosal layer. In conclusion, the presented results proved the antiulcer potential of SP and A. chinensis extracts against an indomethacin-induced gastric ulcer in rats, which may be due to their antioxidant and anti-inflammation efficiency. Thus, these data suggested that SP, KF, KP, and SFP extracts as natural and safe alternatives have a gastroprotective potential against indomethacin-induced gastric ulceration. The antioxidative and anti-inflammatory properties are probable mechanisms.
Highlights
Gastric ulceration is the most prevalent gastrointestinal disorder accounting for an estimated mortality of 15 out of every 15,000 complications yearly [1]
The current study aims to investigate the possible antiulcerogenic and gastroprotective potential of golden kiwifruit and Spirulina platensis (SP) extracts against an indomethacin-induced gastric ulcer in rats model, which will be be further investiaged for potential application in functional supplements or beverages as well as in dietetic therapy for peptic and duodenum ulcers
Treating rats with SP, kiwifruit (Actinidia chinensis) flesh (KF), kiwifruit peel (KP), and mix of SP+KF+KP in equal volumes (SFP) extracts markedly reduced gastric exudation and volume expansion induced by indomethacin
Summary
Gastric ulceration is the most prevalent gastrointestinal disorder accounting for an estimated mortality of 15 out of every 15,000 complications yearly [1]. With regards to NSAIDs, indomethacin is a nonsteroidal anti-inflammatory drug that was introduced in 1963 to treat inflammatory diseases [6]. It is readily absorbed from the gastrointestinal tract almost entirely after oral ingestion and is metabolized by the liver and converted to active metabolites [7]. The clinical use of indomethacin is associated with potentially life-threatening deleterious effects as gastrointestinal ulceration, bleeding [8], renal toxicity [9], hepatic injury [10], intestinal damage, anemia, and the loss of protein [11]. The administration of indomethacin results in serious adverse effects on the cardiovascular system [12], initiation of lipid peroxidation, the elevation of oxidative stress [13], and infiltration of inflammatory cells [14]
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