[Corrigendum] Protective effect of angiotensin­(1­7) against hyperglycaemia­induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway.

Subsequently to the publication of this article, the authors have realized that an address affiliation associated with certain of the authors had been omitted. The authors' affiliation information should have appeared as follows (the omitted address affiliation is featured in bold): Yi­Ying Yang1,2*, Xiu­Ting Sun1,2*, Zheng­Xun Li1,2, Wei­Yan Chen3, Xiang Wang4, Mei­Ling Liang5, Hui Shi1,2, Zhi­Sheng Yang1,2 and Wu­Tao Zeng1,2 1Department of Cardiology, The First Affiliated Hospital, Sun Yat­Sen University; 2Key Laboratory on Assisted Circulation, Ministry of Health, Guangzhou, Guangdong 510080; 3Intensive Care Unit, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510260; 4Department of Cardiology, Laiwu City People's Hospital, Laiwu, Shandong 27110; 5Department of Cardiology, Sun Yat­Sen Cardiovascular Hospital, Shenzhen, Guangdong 518020, P.R. China *Contributed equally. The authors regret this error in the affiliations, and apologize for any inconvenience caused. [the original article was published in the International Journal of Molecular Medicine 41: 1283­1292, 2018; DOI: 10.3892/ijmm.2017.3322].

Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway.

Angiotensin-(1-7) [Ang-(1-7)], a heptapeptide mainly generated from cleavage of AngⅠ and AngⅡ, possesses physiological and pharmacological properties, including anti­inflammatory and antidiabetic properties. Activation of the phosphoinositide 3-kinase and protein kinase B (PI3K̸Akt) signaling pathway has been confirmed to participate in cardioprotection against hyperglycaemia-induced injury. The aim of the present study was to test the hypothesis that Ang-(1-7) protects H9c2 cardiomyoblast cells against high glucose (HG)-induced injury by activating the PI3K̸Akt pathway. To examine this hypothesis, H9c2 cells were treated with 35 mmol/l (mM) glucose (HG) for 24 h to establish a HG-induced cardiomyocyte injury model. The cells were co-treated with 1 µmol/l (µM) Ang-(1-7) and 35 mM glucose. The findings of the present study demonstrated that exposure of H9c2 cells to HG for 24 h markedly induced injury, as evidenced by an increase in the percentage of apoptotic cells, generation of reactive oxygen species and level of inflammatory cytokines, as well as a decline in cell viability and mitochondrial luminosity. These injuries were significantly attenuated by co-treatment of the cells with Ang-(1-7) and HG. In addition, PI3K̸Akt phosphorylation was suppressed by HG treatment, but this effect was abolished when the H9c2 cells were co-treated with Ang-(1-7) and HG. Furthermore, the cardioprotection of Ang-(1-7) against HG-induced injury in H9c2 cardiomyoblasts was highly attenuated in the presence of either D-Ala7-Ang-(1-7) (A-779, an antagonist of the Mas receptor) or LY294002 (an inhibitor of PI3K̸Akt). In conclusion, the present study provided new evidence that Ang-(1-7) protects H9c2 cardiomyoblasts against HG-induced injury by activating the PI3K̸Akt signaling pathway.

[Quality of life in patients with chronic hepatitis C after PEG-Interferon a-2a therapy].

OBJECTIVE: To evaluate the quality of life (QOL) in the patients with chronic hepatitis C (CHC) after PEG-Interferon a-2a therapy. METHODS: A study based on 102 CHC patients (group A, before PEG- Interferon a-2a therapy, T0) and 44 healthy persons (group B) was carried out using the general quality of life inventory (GQOLI-74) questionnaire, and QOL were compared between the two groups. Patients in group A were divided into subgroup A1 (72 patients ) which was given PEG-Interferon a-2a plus Ribavirin for one year and subgroup A2 (30 patients) without any antivirus therapy. QOL of patients in these two subgroups was investigated using GQOLI-74 questionnaire on the end of PEG-Interferon a-2a plus Ribavirin therapy (T1) and half one year after the end of PEG-Interferon a-2a plus Ribavirin therapy (T2). QOL of CHC patients (group A1 and A2) were compared at T0, T1 and T2, respectively. RESULTS: Compared with group B, patients in group A had lower QOL (P < 0.05) on other scales and total scores of the GQOLI-74 questionnaire except psychological function(P > 0.05). Both on T1 and T2, patients in subgroup A1 had higher QOL on physical function, psychological function, social function and total scores than patients in subgroup A2 at the same time (P < 0.05). Patients in subgroup A1 at T1 had higher QOL on physical function, psychological function, social function and total scores than at T0 (P < 0.05). Patients in subgroup A1 at T2 had higher QOL on social function than that at T1 (P < 0.05). CONCLUSIONS: QOL of CHC patients is more impaired than healthy persons. PEG-Interferon a-2a therapy will improve the QOL.