The effect of metyrosine on oxidative gastric damage induced by ischemia/reperfusion in rats. Biochemical and histopathological evaluation

Cimen, Orhan; Çimen, Ferda Keskin; Gülaboğlu, Mine; Bilgin, Asli Ozbek; Çekiç, Arif Burak; Eken, Huseyin; Süleyman, Zeynep; Bilgin, Yasin; Altuner, Durdu

doi:10.1590/s0102-865020180030000008

Cited by 7 publications

(5 citation statements)

References 27 publications

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“…In the previous study, I/R was found to cause pathological damage like necrosis, hemorrhage, edema, leukocyte infiltration and dilated congested blood vessels in the gastric mucosa [31]. The disappearance of pathological findings in the taxifolin group may be due to its antioxidant activity.…”

Section: Discussionmentioning

confidence: 76%

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Biochemical and histopathological evaluation of taxifolin: An experimental study in a rat model of liver ischemia reperfusion injury

Eken¹,

Kurnaz²

2019

Journal of Surgery and Medicine

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Aim: Ischemia/reperfusion (I/R) procedure applied during liver resection and transplantation in clinic settings causes liver oxidative damage. The aim of this study was to examine the effects of taxifolin on liver injury induced by I/R in rats. Methods: Albino Wistar male rats divided into three groups with 6 rats in each group: liver ischemia-reperfusion (LIR), 50 mg/kg taxifolin + liver ischemia reperfusion (TLIR) and sham operation (SHAM). An hour before thiopental sodium anesthesia, 50 mg/kg taxifolin was orally administered to the TLIR group and distilled water to the LIR and SHAM groups. In the TLIR and LIR groups, a clamp was placed in the hepatic artery, portal vein and bile duct, thereby inducing ischemia for one hour, and reperfusion for six hours. In the SHAM group, the abdominal cavity was closed by surgical suture without any procedure. At the end of this period, rats were sacrificed with high dose anesthesia. Liver tissues were removed for biochemical and histopathological examinations Results: I/R procedure significantly increased MDA (P<0.001), ALT, AST levels (P<0.001) and decreased tGSH level (P<0.001) in liver tissue compared to SHAM group. In the taxifolin treated group, this effect was suppressed. Histopathologically, in the I/R induced group, pathological findings such as dilated congested blood vessel, hemorrhage, destruction in the liver parenchyma and edema observed. Liver tissue in the taxifolin group had nearnormal appearance except mild sinusoidal congestion. Conclusion: Our results indicate that taxifolin is an effective agent in reducing hepatic damage caused by I/R.

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Section: Discussionmentioning

confidence: 76%

“…The disappearance of pathological findings in the taxifolin group may be due to its antioxidant activity. Antioxidant activity has been shown to be important in reducing I/R damage [31,32].…”

Section: Discussionmentioning

confidence: 99%

Biochemical and histopathological evaluation of taxifolin: An experimental study in a rat model of liver ischemia reperfusion injury

Eken¹,

Kurnaz²

2019

Journal of Surgery and Medicine

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“…Our results showed that I/R procedure significantly increased MDA level in gastric tissue compared to SHAM and taxifolin group. Our previous experimental study also presented that I/R procedure elevated MDA level in animal gastric tissue 4 . As it is known, MDA is last molecule of lipid peroxidation (LPO), also a good marker to evaluate oxidative tissue damage 21 .…”

Section: Discussionmentioning

confidence: 90%

“…One of the product of oxidative DNA damage is 8 hydroxyguanine (8-OHGua) and is used as an important parameter in determining oxidative stress 3 . In recent studies, the roles of increase in MDA production and decrease in total glutathione (tGSH) production have been shown in the pathogenesis of gastric ischemia-reperfusion (I/R) injury 4 . Polat et al 5 .…”

Section: Introductionmentioning

confidence: 99%

Effect of taxifolin on oxidative gastric injury induced by celiac artery ligation in rats

et al. 2019

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Purpose: To examine the effect of taxifolin on I/R induced gastric injury in rats using biochemical and histopatholohical methods. Methods: Eighteen albino Wistar male rats equally grouped as; gastric I/R (I/R), 50 mg/kg taxifolin + gastric I/R (TAX+ I/R) and sham operation applied (SHAM). Ischemia induced for 1 hour, and reperfusion induced for 3 hours. Results: Oxidant parameters like, Malondialdehyde (MDA) and Hydroxyguanine (8-OHdG) were higher, whereas total glutathione (tGSH) was lower in the I/R group according to SHAM group, histopathological findings such as marked destruction, edema, and proliferated dilated congested blood vessels were observed severely in the I/R group, whereas there was not any pathological finding except mild dilated congested blood vessels in the TAX+ I/R group. Conclusion: The taxifolin can be clinically beneficial in the treatment of gastric injury due to I/R procedure.

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“…Consistently, previous reports have suggested that AMPT ameliorates oxidative stress and inflammation in other pathological settings. 42,43 Noteworthy, these vascular effects were associated to the downregulation of TH in AMPT-treated animals. Therefore, our data indicate that TH upregulation negatively impacts on AAA formation and support the potential of targeting this enzyme in AAA.…”

Section: Discussionmentioning

confidence: 99%

Targeting Tyrosine Hydroxylase for Abdominal Aortic Aneurysm: Impact on Inflammation, Oxidative Stress, and Vascular Remodeling

et al. 2021

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Pharmacological treatments for preventing abdominal aortic aneurysm (AAA) rupture or slowing aneurysm progression remain a challenge. It is increasingly recognized that sympathetic activity might play a role in the pathogenesis of AAA; however, the impact of this pathway remains unclear. Here, we show that the expression of tyrosine hydroxylase ( TH ), dopamine β-hydroxylase ( DBH ), and the norepinephrine transporter SLC6A2 is upregulated in abdominal aorta samples from AAA patients and in the aneurysmal aorta from 2 animal models susceptible to Ang II (angiotensin II)–induced AAA: the apolipoprotein E-deficient (ApoE −/− ) model and a transgenic mouse that overexpresses the human nuclear receptor NOR-1 (neuron-derived orphan receptor-1) in the vascular wall (TgNOR-1 VSMC ). TH localizes to sympathetic nerves innervating the local vasculature, but also to inflammatory cells, and scattered vascular smooth muscle cell in human and mouse AAA. Interestingly, the preventive effect of doxycycline on AAA formation in Ang II–treated TgNOR-1 VSMC mice was associated to the normalization of vascular Th expression. Moreover, the TH specific inhibitor α-methyl- p -tyrosine protected against Ang II–induced AAA formation, limiting the progressive increase in aortic diameter without affecting blood pressure. The drug normalized MMP2 (matrix metalloproteinase 2) expression and MMP activity, preserving elastin integrity, attenuated the Ang II–mediated rise in vascular oxidative stress and inflammatory markers and reduced the inflammatory infiltrate. Finally, NOR-1, whose expression correlated with that of TH in human AAA, was able to drive human TH transcriptional activity in transient transfection assays. Therefore, the upregulation of the TH pathway could be critical in the pathophysiology of AAA, supporting the potential of pharmacological strategies targeting TH for AAA management.

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The effect of metyrosine on oxidative gastric damage induced by ischemia/reperfusion in rats. Biochemical and histopathological evaluation

Abstract: Metyrosine prevented the I/R induced oxidative stress in the gastric tissue. Metyrosine may be beneficial for gastric I/R injury.

Cited by 7 publications

References 27 publications

Biochemical and histopathological evaluation of taxifolin: An experimental study in a rat model of liver ischemia reperfusion injury

Biochemical and histopathological evaluation of taxifolin: An experimental study in a rat model of liver ischemia reperfusion injury

Effect of taxifolin on oxidative gastric injury induced by celiac artery ligation in rats

Targeting Tyrosine Hydroxylase for Abdominal Aortic Aneurysm: Impact on Inflammation, Oxidative Stress, and Vascular Remodeling

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