Effects of leptin on stress-induced changes of caspases in rat gastric mucosa

Ercan, Sevim; Özer, Çiğdem; Tas, Murat; Erdoğan, Deniz; Babül, Aydan

doi:10.1007/s00535-007-2032-1

Cited by 5 publications

(3 citation statements)

References 53 publications

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“…Another study demonstrated that sodium bisulfite and sodium sulfite at various doses (125, 250 or 500 mg/kg body weight) significantly increase DNA damage on stomach and different organs (Meng et al, 2004). Our previous study also showed that cold-restraint stress caused apoptosis in gastric mucosa secondary to a decrease in antioxidant capacity and an increase in oxidant activity (Ercan et al, 2007). Recent studies showed that indomethacin and helicobacter pylori induce mitochondrial pathology that ultimately activates the mitochondrial pathway of apoptosis in gastric mucosa to develop gastropathy (CalvinoFernandez et al, 2008;Maity et al, 2009).…”

Section: Discussionmentioning

confidence: 87%

Sodium metabisulfite induces lipid peroxidation and apoptosis in rat gastric tissue

et al. 2010

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Sodium metabisulfite (Na( 2)S(2)O(5)) is used as an antioxidant and antimicrobial agent in a variety of drugs and functions as a preservative in many food preparations. This study was performed to elucidate the dose-dependent effects of sodium metabisulfite ingestion on rat gastric tissue apoptotic changes and lipid peroxidation. Forty male wistar rats, aged 3 months were used. They were randomly divided into four groups: control (C), the group treated with Na(2)S(2)O(5) (10 mg/kg; S1), the group treated with Na(2)S(2)O(5) (100 mg/kg; S2), the group treated with Na(2)S(2)O(5) (260 mg/kg; S3). Na( 2)S(2)O(5) was given by intragastric intubation for 35 days. In the S2 and S3 groups, malondialdehyde (MDA) levels increased markedly when compared with the control group. High doses of sulfite administration elevated number of apoptotic cells both in mucosa and submucosa layers of stomach in parallel with increased MDA levels. These results suggest that sodium metabisulfite increased lipid peroxidation and thus number of apoptotic cells on gastric tissue in dose-dependent manner.

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Section: Discussionmentioning

confidence: 87%

Sodium metabisulfite induces lipid peroxidation and apoptosis in rat gastric tissue

et al. 2010

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“…Stressors of different types [25][26][27][28] or treatments with glucocorticoids [29][30][31][32] induce apoptosis in different tissues, including testicular germ cells [33]. Fluid from follicles of women whose oocytes were not fertilized contained cortisol levels significantly higher than in the fluid from follicles containing successfully fertilized oocytes [34].…”

Section: Introductionmentioning

confidence: 99%

Restraint Stress Impairs Oocyte Developmental Potential in Mice: Role of CRH-Induced Apoptosis of Ovarian Cells1

Liang

Wei

Cheng

et al. 2013

Biology of Reproduction

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This study examined the role of CRH-induced ovarian cell apoptosis in the restraint stress (RS)-induced impairment of oocyte competence. Oocyte percentages of apoptotic cumulus cells (CCs) did not differ between stressed and control mice before in vitro maturation (IVM) but became significantly higher in stressed mice after IVM without serum, growth factor, and hormone. The level of Bcl2 mRNA decreased significantly in mural granulosa cells (MGCs) and ovarian homogenates after RS. Whereas ovarian estradiol, testosterone, and IGF1 decreased, cortisol and progesterone increased significantly following RS. RS increased the level of CRH in serum, ovary, and oocyte while enhancing the expression of CRHR1 in CCs, MGCs, and thecal cells. RS down-regulated ovarian expression of glucocorticoid receptor and brain-derived neurotrophic factor. Furthermore, CRH supplementation to IVM medium impaired oocyte developmental potential while increasing apoptotic CCs, an effect that was completely overcome by addition of the CRHR1 antagonist antalarmin. Results suggest that RS impaired oocyte competence by increasing CRH but not glucocorticoids. Increased CRH initiated a latent apoptotic program in CCs and oocytes during their intraovarian development, which was executed later during IVM to impair oocyte competence. Thus, elevated CRH interacted with increased CRHR1 on thecal cells and MGCs, reducing the production of testosterone, estrogen, and IGF1 while increasing the level of progesterone. The imbalance between estrogen and progesterone and the decreased availability of growth factors triggered apoptosis of MGCs and facilitated CC expression of CRHR1, which interacted with the oocyte-derived CRH later during IVM to induce CC apoptosis and reduce oocyte competence.

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“…The ischemic condition caused an increase in the level of H 2 O 2 , which, in conjugation with O 2 generates OH. Lipid peroxidation induced by oxygen-free radicals seems to play a critical role in the pathogenesis of acute gastric mucosal injury in both experimental animals and humans [32]. Oxidative stress and caspases have been implicated as potential mediators of cell death [30].…”

Section: Discussionmentioning

confidence: 99%

Possible protective effect of gum arabic on experimentally induced gastric ulcer in adult male albino rats

Helal¹,

Yousef²,

El-Naa³

2011

The Egyptian Journal of Histology

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Effects of leptin on stress-induced changes of caspases in rat gastric mucosa

Abstract: Cold-restraint stress decreases the antioxidant capacity of stomach tissue while activating oxidants, and induces apoptosis by an increase in caspase immunoreactivity. The presence of leptin reverses these mechanisms and suppresses the apoptosis.

Cited by 5 publications

References 53 publications

Sodium metabisulfite induces lipid peroxidation and apoptosis in rat gastric tissue

Sodium metabisulfite induces lipid peroxidation and apoptosis in rat gastric tissue

Restraint Stress Impairs Oocyte Developmental Potential in Mice: Role of CRH-Induced Apoptosis of Ovarian Cells1

Possible protective effect of gum arabic on experimentally induced gastric ulcer in adult male albino rats

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