scholarly journals Lupeol Stearate Accelerates Healing and Prevents Recurrence of Gastric Ulcer in Rodents

Author(s):  
Lincon Bordignon Somensi ◽  
Philipe Costa ◽  
Thaise Boeing ◽  
Luisa Nathalia Mariano ◽  
Elizama Gregório ◽  
...  

Abstract The gastric healing and gastric ulcer recurrence preventive effect of Lupeol Stearate (LS) was measured in this study. To evaluate the gastric healing effect, rats were submitted to the 80% acetic acid-induced ulcer model and treated with vehicle (1 ml/kg, p.o.), LS (1 mg/kg, p.o.) or omeprazole (20 mg/kg, p.o.) twice a day for seven days. The gastric injury was evaluated macroscopically, histologically and histochemical; and biochemical parameters were also quantified. To evaluate the effects of LS on gastric ulcer recurrence, mice were ulcerated by gastric instillation of 10% acetic acid and treated with vehicle (1 ml/kg, p.o.), LS (1 mg/kg, p.o.) or ranitidine (20 mg/kg, p.o.) twice a day for ten days. Then, the ulcer recurrence in these animals was induced by IL- 1β (1 µg/kg i.p) at five day after the end of the treatment period. The area of the lesion recurred were measured, as well as the activity of myeloperoxidase and TNF levels. Oral treatment with LS accelerated gastric healing by 63% compared to the group treated with vehicle, which was also evidenced by histological improvement and increased production of mucin in the gastric epithelium. LS elevated the activity of the glutathione S-transferase and reduced the activity of myeloperoxidase, but did not change the levels of reduced glutathione or the activity of superoxide dismutase and catalase at the ulcer site in rats. Regarding the recurrence, the LS treatment reduced the recurred lesions, reducing MPO activity but not TNF levels at ulcer site. It can be concluded that LS promotes the healing of gastric lesions by favoring the mucus production and reducing the migration of neutrophils and that it can reduce the severity of the ulcer recurrence.

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
A. Folorunsho Ajayi ◽  
S. Babafemi Olaleye

Cell proliferation and angiogenesis are of utmost importance for healing to take place. The KI67 and EGFR proteins are markers of cell proliferation, while CD31 and factor VIII are markers of angiogenesis. To elucidate the mechanism responsible for delayed healing of the gastric injury in old age, we analyzed the expression of these markers in rats of different months during the healing of an acetic acid-induced gastric ulcer. Male Wistar rats (aged 3, 6, 12, and 18 months) divided into four groups, according to their ages, formed the experimental animals. Stomach tissue samples were collected on days 3, 7, 14, and 21 after induction for assessment of ulcer healing. The area of gastric mucosa healed was inversely proportional to age. The expression of markers of proliferation (KI67 and EGFR) and angiogenesis (factor VIII and CD31) decreased significantly (p<0.05) in older rats when compared with younger ones (3 months > six months > 12 months > 18 months) on days 7, 14, and 21 after induction of gastric ulcer. This study revealed that the slower gastric ulcer healing rate in older rats might be due to reduced epithelial cell proliferation and angiogenic activities.


2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Xueying Zhao ◽  
Ji Li ◽  
Yonghai Meng ◽  
Mingming Cao ◽  
Jianwei Wang

Jinlingzi powder comprises Melia toosendan Sieb. et Zucc. and Corydalis yanhusuo (Y.H. Chou & Chun C.Hsu) W.T. Wang ex Z.Y. Su & C.Y. Wu and is usually applied in clinic as traditional Chinese medicine for pain. The present study aims to investigate the therapeutic actions of Jinlingzi powder and its extracted components and theirs treatment mechanism on the acetic acid induced-gastric ulcer in rats. The gastric ulcer model was induced by the administration of acetic acid in rats (84 male). Jinlingzi powder water decoction, its polysaccharide, and nonalkaloid and alkaloid components were used to investigate the therapeutic actions on the acetic acid induced-gastric ulcer by measuring the related pharmacy and pharmacodynamic factors, including ulcer index, ulcer area, ulcer healing rate, interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), neurotensin (NT), platelet activating factor (PAF), thromboxane B2 (TXB2), and vascular endothelial growth factor (VEGF) in rat serum, acetylcholinesterase (AChE) in brain tissue, prostaglandin E2 (PGE2), and basic fibroblast growth factor (bFGF) in gastric tissue. Among the various groups, Jinlingzi powder and the nonalkaloid components caused significant changes in IL-8, TNF-α, NT, PAF TXB2, and VEGF values in the serum. The AChE content in the rats’ brain tissue was also reduced after using Jinlingzi powder and the nonalkaloid components. Additionally, Jinlingzi powder and the nonalkaloid components considerably affect the amount of PGE2 and bFGF in a rat’s stomach tissue. Therefore, Jinlingzi powder and the nonalkaloid components can effectively inhibit neutral neutrophil activation, prevent capillaries thrombosis, and protect gastric mucosa. Thus, the nonalkaloid components of the Jinlingzi powder play a key role in the treatment of gastric ulcer.


2014 ◽  
Vol 675-677 ◽  
pp. 126-129 ◽  
Author(s):  
Shu Jing ◽  
Wei Hai Jiang ◽  
Wei Sun

In this study, SD rats were used to establish an acetic acid-induced rat gastric ulcer model, and SOD and GSH-PX activities and MDA contents in rats with the gastric ulcer induced by acetic acid were measured. The results showed that smoking could delay the healing of gastric ulcer induced by acetic acid and aggravate the ulceration; compared with those in the model group, serum SOD, GSH-PX activities were significantly reduced, and MDA levels were significantly elevated, in rats with the gastric ulcer induced by acetic acid, suggesting that smoking may reduce the body's antioxidant capacity. The results indicate that smoking may induce or aggravate gastric ulcer by reducing the activity of serum SOD and GSH-PX, and elevating the content of serum MDA in rats with acetic acid-induced gastric ulcer, to affect the metabolism of oxygen free radicals to cause the oxidative damage.


2008 ◽  
Vol 42 (3) ◽  
pp. 204-214 ◽  
Author(s):  
Tae Young Oh ◽  
Byung Ok Ahn ◽  
Eun Jung Jang ◽  
Joo Sang Park ◽  
Sang Jong Park ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A153-A153
Author(s):  
S MIYAMOTO ◽  
K KATO ◽  
Y ISHII ◽  
S ASAI ◽  
T NAGAISHI ◽  
...  

Planta Medica ◽  
2009 ◽  
Vol 75 (09) ◽  
Author(s):  
FM de-Faria ◽  
A Luiz-Ferreira ◽  
ACA Almeida ◽  
V Barbastefano ◽  
MA Silva ◽  
...  

Planta Medica ◽  
2013 ◽  
Vol 79 (13) ◽  
Author(s):  
S Mahattanadul ◽  
S Nima ◽  
S Tewtrakul ◽  
P Tansakul

1996 ◽  
Vol 71 ◽  
pp. 202
Author(s):  
Kouichirou Wada ◽  
Yoshinori Kamisaki ◽  
Masayuki Kitano ◽  
Yosuke Kishimoto ◽  
Kentaro Nakamoto ◽  
...  

2021 ◽  
Author(s):  
Priscilla Maiselina Sriepindonnta ◽  
Fatimah Nur Fitriani ◽  
Savannah Quila Thirza ◽  
Made Dinda Pratiwi ◽  
Dwi Evan Prima Putra Noviardi ◽  
...  

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