Abstract
Ophiopogonin, including Ophiopogonin A, B, C, D, is an effective active component of traditional Chinese medicine Ophiopogon japonicus which has a wide range of pharmacological effects such as protecting myocardial ischemia, resisting myocardial infarction, immune regulation, lowering blood glucose, and anti-tumor. However, the functions of ophiopogonin A on hemorrhagic shock (HS)-induced renal injury remain unclear. First, this study constructed an HS rat model and hypoxia HK-2 cell model to assess the effects of ophiopogonin A in vivo and in vitro. In vivo, HE and TUNEL staining show that ophiopogonin A dose-dependently inhibits HS-induced tissue damage and apoptosis. Moreover, ophiopogonin A dose-dependently downregulates the levels of blood urea nitrogen (BUN), creatinine (Cr), KIM-1, NGAL, iNOS, TNF-α, IL-1β, and IL-6 in HS rats kidney tissues, and decreases the number of MPO-positive cells. In vitro, we get similar results that ophiopogonin A dose-dependently improves hypoxia-induced HK-2 cell apoptosis and damage. In addition, ophiopogonin A dose-dependently increases the expression of NF E2-related factor 2 (Nrf2), while knockdown of Nrf2 reverses the functions of ophiopogonin A in vivo and in vitro. Furthermore, ophiopogonin A dose-dependently promotes the phosphorylation of ERK in HS kidney tissues and hypoxia-treated HK-2 cells, suggesting that ophiopogonin A functions via the p-ERK/ERK signaling pathway.
Highlights
Hemorrhagic shock (HS) is one of a number of critical clinical situations that can be caused by trauma or major surgery
There was no significant difference in the levels of blood urea nitrogen (BUN) and Cr between sham + vehicle and Sham + ophiopogonin A high C group (Figure 1C)
The levels of serum BUN and Cr were increased in the HS group, which were pronouncedly reversed by ophiopogonin A, especially in high concentrations (Figure 1C)
Summary
Hemorrhagic shock (HS) is one of a number of critical clinical situations that can be caused by trauma or major surgery. A decrease in blood perfusion in multiple tissues and organs across the whole body is caused by HS, which leads to complications and a high mortality rate (Mitra et al, 2014; Hamada et al, 2020). It has been reported that severe hemorrhage creates sympathetic nerve excitement, which leads to a significant reduction in renal blood perfusion, causing renal ischemia and hypoxia, resulting in acute kidney injury (AKI) and accelerating the death of Ophiopogonin A Alleviates Renal Injury via Nrf the patient (Wu et al, 2020). AKI is a common clinical disease, especially in critically ill patients who have undergone major surgery, developed sepsis, experienced trauma, cardiogenic shock, hypovolemia, or used nephrotoxic drugs. It is essential to develop new treatment strategies for renal injuries caused by HS
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
