Anti-apoptosis effect of heme oxygenase-1 on lung injury after cardiopulmonary bypass

Wei, Sheng; Yang, Haiqin; Niu, Zhaozhuo; Yin, Hong

doi:10.21037/jtd.2020.03.48

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…So, we can assume that this increase in anti-apoptotic Bcl-2 proteins may be provoked at least in part, by an increase in HO-1 activity. In consistent with our results, Sheng et al reported that HO-1 could reduce and inhibit apoptosis of lung tissue during cardio-pulmonary bypass in rats, and its anti-apoptotic effect may be achieved by upregulating the expression of anti-apoptotic protein bcl-2 in lung tissue [ 43 ]. Several other studies also confirmed upregulation of Bcl-2 [ 44 , 45 , 46 ] and heme oxygenase [ 47 ] in renal I/R injury model.…”

Section: Discussionsupporting

confidence: 92%

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

Ostojic

Ivanov

Mihailović-Stanojević

et al. 2021

IJMS

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Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.

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Section: Discussionsupporting

confidence: 92%

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

Ostojic

Ivanov

Mihailović-Stanojević

et al. 2021

IJMS

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“…Furthermore, h-PGDS overexpression increased the expression of HO-1 and RosA upregulated HO-1 expression in a h-PGDS-dependent manner. HO-1 and its downstream products (Fe 2+ , CO, and biliverdin/bilirubin) could suppress apoptosis triggered by various stimulations or viruses [ 51 , 52 ]. Therefore, the apoptotic effects of RosA might be associated with h-PGDS-dependent HO-1 upregulation.…”

Section: Discussionmentioning

confidence: 99%

Rosmarinic acid treatment protects against lethal H1N1 virus-mediated inflammation and lung injury by promoting activation of the h-PGDS-PGD2-HO-1 signal axis

Zhou,

Wang,

Yang

et al. 2023

Chin Med

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Background Rosmarinic acid (RosA) is a natural phenolic compound that possesses a wide-range of pharmacological properties. However, the effects of RosA on influenza A virus-mediated acute lung injury remain unknown. In this study, we aimed to explore whether RosA could protect against H1N1 virus-mediated lung injury and elucidate the underlying mechanisms. Methods Mice were intragastrically administered with RosA for 2 days before intranasal inoculation of the H1N1 virus (5LD50) for the establishment of an acute lung injury model. At day 7 post-infection (p.i.), gross anatomic lung pathology, lung histopathologic, and lung index (lung weight/body weight) were examined. Luminex assay, multiple immunofluorescence and flow cytometry were performed to detect the levels of pro-inflammatory cytokines and apoptosis, respectively. Western blotting and plasmid transfection with hematopoietic-type PGD2 synthase (h-PGDS) overexpression were conducted to elucidate the mechanisms. Results RosA effectively attenuated H1N1 virus-triggered deterioration of gross anatomical morphology, worsened lung histopathology, and elevated lung index. Excessive pro-inflammatory reactions, aberrant alveolar epithelial cell apoptosis, and cytotoxic CD8+ T lung recruitment in the lung tissues induced by H1N1 virus infection were observed to be reduced by RosA treatment. In vitro experiments demonstrated that RosA treatment dose-dependently suppressed the increased levels of pro-inflammatory mediators and apoptosis through inhibition of nuclear factor kappa B (NF-κB) and P38 MAPK signaling pathways in H1N1 virus-infected A549 cells, which was accompanied by promoting activation of the h-PGDS-PGD2-HO-1 signal axis. Furthermore, we strikingly found that h-PGDS inhibition significantly abrogated the inhibitory effects of RosA on H1N1 virus-mediated activation of NF-κB and P38 MAPK signaling pathways, resulting in diminishing the suppressive effects on the increased levels of pro-inflammatory cytokines and chemokines as well as apoptosis. Finally, suppressing h-PGDS prominently abolished the protective effects of RosA on H1N1 virus-mediated severe pneumonia and lung injury. Conclusions Taken together, our study demonstrates that RosA is a promising compound to alleviate H1N1 virus-induced severe lung injury through prompting the h-PGDS-PGD2-HO-1 signal axis.

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“…Recent findings have demonstrated that apoptosis, a form of programmed cell death, plays an important role in CPB [ 33 , 34 ]. Xu et al showed that pretreatment of Xuebijing injection further reduced the apoptosis of type II alveolar epithelial cells after CPB [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

XueFu ZhuYu Decoction Alleviates Cardiopulmonary Bypass-Induced NLRP3 Inflammasome-Dependent Pyroptosis by Inhibiting IkB-α/NF-κB Pathway in Acute Lung Injury Rats

Zhang

Lou

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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XueFu ZhuYu Decoction (XFZYD) is an effective prescription that is widely used to improve blood circulation by removing blood stasis. This study aimed to investigate the effects and the underlying molecular mechanisms of XFZYD on lung pyroptosis in cardiopulmonary bypass- (CPB-) induced acute lung injury (ALI) rats. A rat model of ALI was induced by CPB treatment after XFZYD, Ac-YVAD-CMK, and Bay-11-7082 administration. The respiratory index (RI) and oxygenation index (OI) were determined at each time point. The levels of interleukin (IL)-1β, IL-6, IL-18, and TNF-α in serum and lung were measured by enzyme-linked immunosorbent assays (ELISA). Moreover, the protein levels, neutrophil counts, and total cell of bronchoalveolar lavage fluid (BALF) were detected. Additionally, Myeloperoxidase (MPO) expression was detected by immunohistochemical assay. Lung injury was evaluated with the wet/dry (W/D) ratio and pathologic changes, respectively. Besides, the expression of NLRP3 inflammasome and IkB-α/NF-κB pathway proteins was estimated by immunofluorescence, quantitative real-time PCR (qRT-PCR), and Western blotting assays, respectively. XFZYD pretreatment significantly ameliorated pulmonary ventilation function and reduced the CPB-induced lung histopathological injury, inflammatory cell infiltration in BALF and lung, and the apoptosis of lung cells. Interestingly, XFZYD decreased the CPB-induced NLRP3, ASC, Caspase-1 p20, Pro-GSDMD, GSDMD p30, IL-18, IL-1β p-P65, and p-IKBα mRNA or protein levels in lung tissues in ALI model rats. In summary, these findings suggest that XFZYD effectively mitigates NLRP3 inflammasome-dependent pyroptosis in CPB-induced ALI model rats, possibly by inhibiting the IkB-α/NF-κB pathway in the lung.

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Anti-apoptosis effect of heme oxygenase-1 on lung injury after cardiopulmonary bypass

Cited by 6 publications

References 36 publications

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

Rosmarinic acid treatment protects against lethal H1N1 virus-mediated inflammation and lung injury by promoting activation of the h-PGDS-PGD2-HO-1 signal axis

XueFu ZhuYu Decoction Alleviates Cardiopulmonary Bypass-Induced NLRP3 Inflammasome-Dependent Pyroptosis by Inhibiting IkB-α/NF-κB Pathway in Acute Lung Injury Rats

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