Beraprost Sodium, a Stable Analogue of PGI2, Inhibits the Renin-Angiotensin System in the Renal Tissues of Rats with Chronic Renal Failure
Authors: Xiao-Qing Lu
Bei-Hao Zhang
Xin-Fang Wang
Pei Wang
Journal: Kidney & Blood Pressure Research (2018)
Discipline: CLINICAL MEDICINE
Keywords: Beraprost sodium; Chronic renal failure; Pgi2 analogue; Renin-angiotensin system.

Abstract:  Background/aims: Chronic renal failure (CRF) is a prolonged kidney condition characterized by decreased kidney function that can eventually develop into total kidney failure. The renin-angiotensin system (RAS) helps to regulate the balance between human bodily fluids and electrolytes. The aim of the present study was to investigate the effects of a prostacyclin analogue (beraprost sodium [BPS]) on the expression of key factors associated with local RAS activities in the renal tissues of rats with CRF. Methods: After a CRF rat model was successfully established, the levels of BUN, SCr, phosphorus, and calcium were detected by an automatic biochemistry analyzer. Furthermore, the activities of malondialdehyde (MDA) and superoxide dismutase (SOD) in rat renal tissues were measured using a colorimetric method, while the activity of angiotensin-converting enzyme (ACE) was determined by ultraviolet (UV) spectrophotometry. In situ hybridization was employed to determine the expression of angiotensin II type 1 receptor (AT). Finally, the positive expression rates of cells expressing important apoptotic proteins (Bax and Bcl-2) were determined, and the protein and mRNA levels of phosphatidylinositol 3-kinase (AKT) and key factors involved in the RAS (AT1, AT2, angiotensin ACE and angiotensinogen [AGT]) were evaluated by RT-qPCR and western blot analysis. Results: Initial observations revealed that treatment with BPS decreased the levels of BUN, SCr and phosphorus but increased calcium levels in the renal tissues of CRF rats. Additionally, BPS reduced the levels of MDA while increasing the levels of SOD, ACE activity, and AT1 expression in the renal tissues of CRF rats. BPS inhibited glomerular hypertension and hyperfiltration; increased the mRNA and protein levels of AKT and AT2; and decreased the mRNA and protein levels of AT1, AGT, and ACE in the renal tissues of CRF rats. Conclusion: The results of this study demonstrate that BPS, a PGI2 analogue, inhibits the expression of key factors involved in the local RAS, resulting in a delay in the occurrence and development of CRF. The key findings of the present study ultimately highlight the potential of this PGI2 analogue as a promising therapeutic strategy for treating CRF. 

Retracted: No

PubPeer comments:
 Fig 6C:  RT-qPCR and western blot analysis results revealing that BPS decreases the mRNA and protein levels of AT1, AGT, and ACE and increases the mRNA and protein levels of AT2 in CRF rats. ...C, protein levels of key RAS factors determined by western blot analysis . ![file] The loading control has appeared in a number of other studies with unrelated authors. E.g. Fig 8(a) from [Liu et al (2018)] and Fig. 9A of [Zhou et al (2018)] . More examples in the Zhou et al thread. ![] , 
 #1 6C again, flipped horizontally to emphasise the protein blobs shared with 5B of [Han et al (2018)] . ![] ![] , 
 Retracted [14 October 2021] . ------------------------ The article u201cBeraprost Sodium, a Stable Analogue of PGI2, Inhibits the Renin-Angiotensin System in the Renal Tissues of Rats with Chronic Renal Failureu201d [Kidney Blood Press Res. 2018;43:1231u20131244, DOI: 10.1159 000492405] by Xin-Fang Wang, Bei-Hao Zhang, Xiao-Qing Lu, and Pei Wang has been retracted by the Publisher and the Editor. After the publication of this article, concerns were raised about the integrity of some of the data presented. Specifically, elements of Figure 6c in this article were presented in other articles without justification. The authors did not respond to requests to comment on the concerns and provide the raw data within the given timeframe despite multiple attempts of contact. The matter has been raised to the corresponding authoru2019s institution who did not respond to our request for an investigation. Given the severity of the concerns raised this article is being retracted. In response to our notice of the intention to retract the article, the corresponding author agreed to the retraction. ,