Gastroduodenal mucosal defense

Zhu, Amy; Kaunitz, Jonathan D.

doi:10.1007/s11894-008-0101-0

Cited by 12 publications

(11 citation statements)

References 36 publications

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“…Oral administration of indomethacin (48 mg/kg) and ligation of pylorus produced superficial or deep erosions, bleeding, and antral ulcers. This is similar to the reports of Zhu and Kaunitz [3] and Lanza [68] in which prostaglandin and protective mucus function were inhibited by NSAIDs.…”

Section: Group (N=4)supporting

confidence: 91%

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ANTIULCER ACTIVITY OF Musa paradisiaca (BANANA) TEPAL AND SKIN EXTRACTS IN ULCER INDUCED ALBINO MICE

Ahmad¹

2016

MJAS

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The current use of ulcer drugs is limited due to its side effects and potentiality of relapse. This study aimed to ascertain the antiulcer potentials of the tepal and skin extracts of banana Musa paradisiaca. The parts were processed and extracted using methanol by maceration. Phytochemicals content of both parts were screened. Twenty-five albino mice were used in in vivo analysis. The mice were treated with 100 mg/kg of tepal and skin extract as well as cimetidine for seven days followed by administration of indomethacin. The animals were sacrificed, and the removed stomachs were prepared for the evaluation of ulcer index and gastric wall mucus. pH and volume were measured from the gastric juice. The results revealed that banana's tepal and skin extracts contain phytochemicals like phenols, flavonoids and etc. The tepal and skin extracts prevented the IND+PYL induced ulcer by 68.80 ± 20.53% and 43.22 ± 14.82% respectively. Significant rise (p <0.05) in gastric juice pH (3.79 ± 0.24) was noticed in the banana's tepal treated group. However, the decrease in gastric juice volume and increased gastric wall mucus by both tepal and skin were not statistically significant (p >0.05). Findings from this study shows that banana's tepal and skin were able to prevent IND+PYL induced ulcer by strengthening the gastric mucosa and decreasing the gastric juice acidity.Keywords: banana's tepal, banana's skin, indomethacin, Musa paradisiaca, preventive index Abstrak Penggunaan ubat ulser pada masa kini adalah terhad disebabkan kesan sampingan dan potensi kambuh. Kajian ini bertujuan menentukan potensi antiulser dari ekstrak jantung dan kulit pisang Musa paradisiaca. Bahagian -bahagian ini telah diproses dan diekstrak menggunakan metanol melalui kaedah rendaman. Kandungan fitokimia kedua -dua bahagian telah disaring. Dua puluh lima tikus albino telah digunakan dalam analisis in vivo. Tikus -tikus ini telah diberi rawatan dengan 100mg/kg ekstrak jantung dan kulit pisang serta simetidin selama tujuh hari di ikuti dengan rawatan dengan indomethacin. Haiwan dikorbankan selepas 8 hari rawatan, dan perut dikeluarkan bagi penilaian indeks ulser dan mukus dinding perut. pH dan jumlah jus gastrik juga diukur. Hasil kajian mendapati bahawa ekstrak jantung dan kulit pisang mengandungi beberapa fitokimia seperti fenol, flavonoid, dan lain -lain. Ekstrak jantung dan kulit ini menghalang ulser yang diaruh dengan IND+PYL masing -masing sebanyak 68.80 ± 20.53% dan 43.22 ± 14.82%. Peningkatan yang signifikan (p <0.05) pada pH jus gastrik (3.79 ± 0.24) telah diperhatikan dalam kumpulan yang dirawat dirawat dengan jantung pisang. Walau bagaimanapun, penurunan dalam jumlah jus gastrik dan meningkatkan mukus dinding perut oleh kedua -dua ekstrak adalah tidak signifikan secara statistik (p >0.05). Dapatan dari kajian ini menunjukkan bahawa jantung dan kulit pisang dapat mencegah ulser yang diaruh dengan IND+PYL melalui penambahan mukosa perut dan pengurangan keasidan jus gastrik.

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Section: Group (N=4)supporting

confidence: 91%

“…The etiology of gastro-duodenal (peptic) ulcer has therefore developed when aggressive factors such as, increased HCL and pepsin secretion, parietal cell mass, and gastrin production, dominate the defensive factors (PGs, increased mucous cells etc) [2,3].…”

Section: Introductionmentioning

confidence: 99%

ANTIULCER ACTIVITY OF Musa paradisiaca (BANANA) TEPAL AND SKIN EXTRACTS IN ULCER INDUCED ALBINO MICE

Ahmad¹

2016

MJAS

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“…In addition, AA releases Ca 2+ from intracellular stores and increases mitochondrial uptake of Ca 2+ , which may cause apoptosis [27]. In other cases, prostaglandins, the main byproducts of AA, may be responsible for the protection of some tissues [28,29]. Nevertheless, AA-stimulated oxidative stress has been shown to have a direct effect on mitochondria [1,2].…”

Section: Discussionmentioning

confidence: 99%

Red ginseng abrogates oxidative stress via mitochondria protection mediated by LKB1-AMPK pathway

Dong

Jang

Kang

et al. 2013

BMC Complement Altern Med

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BackgroundKorean ginseng (Panax ginseng C.A. Meyer) has been used as a botanical medicine throughout the history of Asian traditional Oriental medicine. Formulated red ginseng (one form of Korean ginseng) has been shown to have antioxidant and chemopreventive effects.MethodsThis study investigated the cytoprotective effects and mechanism of action of Korean red ginseng extract (RGE) against severe ROS production and mitochondrial impairment in a cytotoxic cell model induced by AA + iron.ResultsRGE protected HepG2 cells from AA + iron-induced cytotoxicity by preventing the induction of mitochondrial dysfunction and apoptosis. Moreover, AA + iron-induced production of ROS and reduction of cellular GSH content (an important cellular defense mechanism) were remarkably attenuated by treatment with RGE. At the molecular level, treatment with RGE activated LKB1-dependent AMP-activated protein kinase (AMPK), which in turn led to increased cell survival. The AMPK pathway was confirmed to play an essential role as the effects of RGE on mitochondrial membrane potential were reversed upon treatment with compound C, an AMPK inhibitor.ConclusionsOur results demonstrate that RGE has the ability to protect cells from AA + iron-induced ROS production and mitochondrial impairment through AMPK activation.

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“…PGs coordinate secretion of protective mucus, surfactant, and bicarbonate, reduce acid secretion, decrease epithelial permeability, increase mucosal blood flow, and enhance inflammation [9], [10]. Although it was hypothesized that selective inhibition of COX-2 could control pain while preventing adverse effects, COX-2-specific NSAIDs still have GI toxicity [11], [12] and they also increase risk of cardiovascular events [13]–[15].…”

Section: Introductionmentioning

confidence: 99%

Mast Cells Are Critical for Protection against Peptic Ulcers Induced by the NSAID Piroxicam

Hampton

Hale

2011

PLoS ONE

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Many commonly used non-steroidal anti-inflammatory drugs (NSAIDs) also cause gastrointestinal toxicity, including the development of life-threatening peptic ulcers. We report that mast cell-deficient mice have an extremely high incidence of severe peptic ulceration when exposed to the NSAID piroxicam. This enhanced ulcer susceptibility can be reversed by reconstitution with mast cells. Furthermore, wild type mice treated with diphenhydramine hydrochloride, a commonly used antihistamine that blocks histamine H1 receptors, develop a similarly high incidence of peptic ulcers following piroxicam exposure. The protective effect of mast cells is independent of TNF, blockade of H2 receptors, or acid secretion. These data indicate a critical role for mast cells and the histamine that they produce in prevention and/or repair of piroxicam-induced gastric mucosal injury. Additional studies will be required to determine whether this represents a NSAID class effect that can be exploited to develop novel therapeutic strategies to limit the incidence of NSAID-induced side effects in humans.

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Gastroduodenal mucosal defense

Cited by 12 publications

References 36 publications

ANTIULCER ACTIVITY OF Musa paradisiaca (BANANA) TEPAL AND SKIN EXTRACTS IN ULCER INDUCED ALBINO MICE

ANTIULCER ACTIVITY OF Musa paradisiaca (BANANA) TEPAL AND SKIN EXTRACTS IN ULCER INDUCED ALBINO MICE

Red ginseng abrogates oxidative stress via mitochondria protection mediated by LKB1-AMPK pathway

Mast Cells Are Critical for Protection against Peptic Ulcers Induced by the NSAID Piroxicam

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