Protective role of hemeoxygenase-1 in gastrointestinal diseases

Chang, Marisol; Xue, Jing; Sharma, Vishal; Habtezion, Aida

doi:10.1007/s00018-014-1790-1

Cited by 57 publications

(44 citation statements)

References 149 publications

(226 reference statements)

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“…Of note, HO-1 overexpression can be applied in multiple clinical conditions, such as organ transplantation, acute kidney injury, hypertension and atherosclerosis (9–14). Importantly, HO-1 is known to exhibit cytoprotective, anti-inflammatory, anti-proliferative, antioxidant and anti-apoptotic activities, making it a promising therapeutic target for the treatment of inflammatory diseases of the gastrointestinal system (15). Panhematin leads to the rapid induction and activation of pancreatic HO-1, and has potential for use in the treatment of human pancreatitis (16).…”

Section: Introductionmentioning

confidence: 99%

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Xiong

Wang

Yuan

et al. 2016

International Journal of Molecular Medicine

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Reseda odorata L. has long been used in traditional Asian medicine for the treatment of diseases associated with oxidative injury and acute inflammation, such as endotoxemia, acute lung injury, acute myocardial infarction and hepatitis. Luteolin, the main component of Reseda odorata L., which is also widely found in many natural herbs and vege tables, has been shown to induce heme oxygenase-1 (HO-1) expression to exert anti-inflammatory and antioxidant effects. In this study, we aimed to examine the effects of luteolin on mice with severe acute pancreatitis (SAP), and to explore the underlying mechanisms. Cerulein and lipopolysaccharide were used to induce SAP in male Institute of Cancer Research (ICR) mice in the SAP group. The SAP group was divided into 4 subgroups, as follows: the vehicle, luteolin, zinc protoporphyrin (ZnPP) only, and luteolin (Lut) + ZnPP (luteolin plus zinc protoporphyrin treatment) groups. The wet/dry weight ratios, hematoxylin and eosin staining and pathological scores of pancreatic tissues were assessed and compared to those of the control mice. Amylase, lipase, nuclear factor-κB (NF-κB) and myeloperoxidase activities, and malondialdehyde, tumor necrosis factor α (TNFα), interleukin (IL)-6, IL-10 and HO-1 levels, as well as the expression of HO-1 were determined in serum and/or pancreatic tissue samples. SAP was successfully induced in male mice compared to normal control mice. The wet/dry weight ratios, pathological scores, and amylase and lipase activity, as well as the levels of TNFα and IL-6 were significantly reduced in the pancreatic tissues of the mice in the Lut group compared with those of the mice in the vehicle group. The Lut group exhibited a significant increase in HO-1 expression in the pancreas and enhanced serum HO-1 and IL-10 levels compared with the vehicle group. The suppression of HO-1 activity in the ZnPP group significantly abolished the protective effects of luteolin. NF-κB expression in the pancreatic tissues from the mice in the Lut + ZnPP group was significantly increased following the suppression of HO-1 activity. On the whole, our findings demonstrate that luteolin protects mice from SAP by inducing HO-1-mediated anti-inflammatory and antioxidant activities, in association with the suppression of the activation of the NF-κB pathway.

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Section: Introductionmentioning

confidence: 99%

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Xiong

Wang

Yuan

et al. 2016

International Journal of Molecular Medicine

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“…It has been reported in rat models of reflux esophagitis that pretreatment with antioxidative isorhamnetin decreased esophageal lesion score reducing MDA levels, possibly due to the upregulation of the esophageal HO-1 expression [50]. Additionally, in cultured esophageal epithelial cells (EEC), it has been observed that euptailin prevented indomethacin-induced cytotoxicity and upregulated HO-1 expression due to nuclear translocation of transcription factor nuclear factor erythroid 2related factor 2 (Nrf2) and the activation of extracellular signal-regulated kinases (ERKs) and phosphatidylinositol-3kinase (PI3K)/Akt signaling [24,51]. However, possible involvement of HO and CO and their possible interaction in the regulation of oxidative stress in the esophageal mucosa requires further investigations.…”

Section: Co and Oxidation Within Thementioning

confidence: 99%

“…Moreover, this protein was localized in sinusoidal cells of the rat's liver [21]. Interestingly, pharmacological inhibition of HO by zinc protoporphyrin IX resulted in the attenuation of vasoactive intestinal polypeptide-(VIP-) induced low esophageal sphincter relaxation implying that this enzymatic protein contributes to the regulation of the motor activity of the upper GI tract [22][23][24].…”

Section: Introductory Notesmentioning

confidence: 99%

Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

Korbut

Brzozowski

Magierowski

2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress reflects an imbalance between oxidants and antioxidants in favor of the oxidants capable of evoking tissue damage. Like hydrogen sulfide (H2S) and nitric oxide (NO), carbon monoxide (CO) is an endogenous gaseous mediator recently implicated in the physiology of the gastrointestinal (GI) tract. CO is produced in mammalian tissues as a byproduct of heme degradation catalyzed by the heme oxygenase (HO) enzymes. Among the three enzymatic isoforms, heme oxygenase-1 (HO-1) is induced under conditions of oxidative stress or tissue injury and plays a beneficial role in the mechanism of protection against inflammation, ischemia/reperfusion (I/R), and many other injuries. According to recently published data, increased endogenous CO production by inducible HO-1, its delivery by novel pharmacological CO-releasing agents, or even the direct inhalation of CO has been considered a promising alternative in future experimental and clinical therapies against various GI disorders. However, the exact mechanisms underlying behind these CO-mediated beneficial actions are not fully explained and experimental as well as clinical studies on the mechanism of CO-induced protection are awaited. For instance, in a variety of experimental models related to gastric mucosal damage, HO-1/CO pathway and CO-releasing agents seem to prevent gastric damage mainly by reduction of lipid peroxidation and/or increased level of enzymatic antioxidants, such as superoxide dismutase (SOD) or glutathione peroxidase (GPx). Many studies have also revealed that HO-1/CO can serve as a potential defensive pathway against oxidative stress observed in the liver and pancreas. Moreover, increased CO levels after treatment with CO donors have been reported to protect the gut against formation of acute GI lesions mainly by the regulation of reactive oxygen species (ROS) production and the antioxidative activity. In this review, we focused on the role of H2S and NO molecular sibling, CO/HO pathway, and therapeutic potential of CO-releasing pharmacological tools in the regulation of oxidative stress-induced damage within the GI tract with a special emphasis on the esophagus, stomach, and intestines and also two solid and important metabolic abdominal organs, the liver and pancreas.

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“…CO, one of the products of HO-1, exhibits anti-inflammatory activity (by downregulation of proinflammatory cytokines, as for instance interleukin-1b (IL-1b), IL-6, and tumor necrosis factor-a, TNF-a), antiapoptotic effects (by downregulation of caspases activation), and anti-proliferative effects by increasing cGMP levels, as reviewed by Ryter et al [45]. Moreover, CO exerts antioxidant actions in several experimental models [46][47][48][49].…”

Section: Antioxidant Capacity Of Phloretin On Brain Cellsmentioning

confidence: 99%

Phloretin‐induced cytoprotective effects on mammalian cells: A mechanistic view and future directions

Oliveira

2016

BioFactors

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Phloretin (C15H14O5), a dihydrochalcone flavonoid, is mainly found in fruit, leaves, and roots of apple tree. Phloretin exerts antioxidant, anti‐inflammatory, and anti‐tumor activities in mammalian cells through mechanisms that have been partially elucidated throughout the years. Phloretin bioavailability is well known in humans, but still remains to be better studied in experimental animals, such as mouse and rat. The focus of the present review is to gather information regarding the mechanisms involved in the phloretin‐elicited effects in different in vitro and in vivo experimental models. Several manuscripts were analyzed and data raised by authors were described and discussed here in a mechanistic manner. Comparisons between the effects elicited by phloretin and phloridzin were made whenever possible, as well as with other polyphenols, clarifying questions about the use of phloretin as a potential therapeutic agent. Toxicological aspects associated to phloretin exposure were also discussed here. Furthermore, a special section containing future directions was created as a suggestive guide towards the elucidation of phloretin‐related actions in mammalian cells and tissues. © 2016 BioFactors, 42(1):13–40, 2016

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Protective role of hemeoxygenase-1 in gastrointestinal diseases

Cited by 57 publications

References 149 publications

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

Phloretin‐induced cytoprotective effects on mammalian cells: A mechanistic view and future directions

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