Gastroprotective Effect of Β3 Adrenoceptor Agonists Zd 7114 and CGP 12177a in Rats

Sevak, Rajkumar J.; Paul, Arindam; Goswami, Sunita; Santani, D. D.

doi:10.1016/s1043661802001500

Cited by 40 publications

(18 citation statements)

References 16 publications

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“…It can decrease stomach-wall friction during peristalsis and provide an effective barrier to back diffusion of hydrogen ions (Sevak et al, 2002). However, gastric wall mucus plays a more important role in the defense of the gastric mucosa against chemical aggression than the soluble mucus in the lumen of the stomach (Allen et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Possible biochemical effects following inhibition of ethanol-induced gastric mucosa damage byGymnema sylvestrein male Wistar albino rats

Al‐Rejaie

Abuohashish²,

Ahmed

et al. 2012

Pharmaceutical Biology

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Section: Discussionmentioning

confidence: 99%

Possible biochemical effects following inhibition of ethanol-induced gastric mucosa damage byGymnema sylvestrein male Wistar albino rats

Al‐Rejaie

Abuohashish²,

Ahmed

et al. 2012

Pharmaceutical Biology

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“…Imidazole is an important pharmacophore in drug discovery. Its derivatives have diverse pharmaceutical effects, including histamine-H3 antagonist (1), anti-inflammatory (2), gastroprotective (3), and antioxidant (4). Importantly, several imidazole derivatives had anticancer activity against a variety of malignant cells.…”

Section: Introductionmentioning

confidence: 99%

Imidazole inhibits autophagy flux by blocking autophagic degradation and triggers apoptosis via increasing FoxO3a-Bim expression

Liu

Wang

Zhao

et al. 2014

International Journal of Oncology

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Abstract. Imidazole, an organic alkaloid, is an important pharmacophore in drug discovery. Anti-neoplastic potential of imidazole derivatives has been documented in several studies; however, mechanisms by which tumor cells respond to these stimuli remain to be elucidated. Autophagy and apoptosis have key roles in tumorigenesis and tumor treatment. In this study, we systematically examined autophagic events induced by imidazole in HEC-1B cells. Accumulation of autophagic vacuoles in imidazole-treated cells was verified by conversion of LC3 protein, as well as confocal and transmission electron microscopy. Furthermore, imidazole blocked autophagic degradation by impairing maturation of autophagosomes into autolysosomes. Concurrently, imidazole treatment induced apoptosis in HEC-1B cells, accompanied by activation of caspase 9 and 3. The proapoptotic effect was mediated by increased Bim expression. Moreover, imidazole upregulated the protein level of Foxo3a and induced its increased nuclear localisation. In addition, siRNA-mediated silencing of FoxO3a effectively attenuated imidazole-induced Bim upregulation and cell death, indicating direct involvement of this pathway in the imidazole-induced apoptosis. Taken together, our data provided a molecular link between imidazoles and anticancer therapies; understanding of these properties of imidazole is essential for development of effective cancer therapeutics using imidazoles.

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“…Imidazole nucleus is an important pharmacophore in drug discovery. Since it is commonly encountered in drugs that display diversity of pharmacological activities such as anti-inflammatory [1], histamine-H3 antagonist [2], antioxidant [3], and gastroprotective [4]. Several imidazole derivatives have shown anticancer activity [5], imidazopyrazine derivatives have shown anticancer activity against Leukemia [6].…”

Section: Introductionmentioning

confidence: 99%

“…5-Substituted 2-Cyanoimino-4-imidazodinone has shown structure-activity relationships against a variety of human cancer cell lines [10]. Bis-pyrrolo [2,1] [1,4]benzodiazepinepyrrole and imidazole compounds have shown anti-tumor activity against nine cancer types [11]. Temozolomide is an alkylating cytostatic drug that finds increasing application in the treatment of melanoma, anaplastic astrocytoma and glioblastoma multiforme [12].…”

Section: Introductionmentioning

confidence: 99%

Pro-apoptotic activity of imidazole derivatives mediated by up-regulation of Bax and activation of CAD in Ehrlich Ascites Tumor cells

et al. 2007

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In this study we report that, imidazole derivatives can induce apoptosis in Ehrlich ascites tumor (EAT) cells, which is clearly evident from annexin-V staining, flow cytometric analysis of cell cycle phase distribution and DNA fragmentation. Delineating further into molecular mechanisms leading to apoptosis of EAT cells, we observed that imidazole derivatives induce tumor cell death by the up-regulation of proto-oncoprotein Bax, release of cytochrome c from the mitochondria which activates caspase-3 and activated caspase-3 activates CAD (Caspase Activated DNase) causes DNA fragmentation. The status of Bcl-2 remains unaltered in EAT cells, and the under expression of Bcl-2 and up-regulation of Bax resulted in the increase of Bax: Bcl-2 ratio suggesting that Bcl-2 family involved in the control of apoptosis. These results suggest a further possible clinical application of imidazole derivatives as pro-apoptotic agent in association with conventional chemotherapeutic agents.

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Gastroprotective Effect of Β3 Adrenoceptor Agonists Zd 7114 and CGP 12177a in Rats

Cited by 40 publications

References 16 publications

Possible biochemical effects following inhibition of ethanol-induced gastric mucosa damage byGymnema sylvestrein male Wistar albino rats

Possible biochemical effects following inhibition of ethanol-induced gastric mucosa damage byGymnema sylvestrein male Wistar albino rats

Imidazole inhibits autophagy flux by blocking autophagic degradation and triggers apoptosis via increasing FoxO3a-Bim expression

Pro-apoptotic activity of imidazole derivatives mediated by up-regulation of Bax and activation of CAD in Ehrlich Ascites Tumor cells

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