RESUMEN
Surface-enhanced Raman scattering (SERS) substrates mostly achieve highly sensitive detection by designing various hot spots; however, how to guide molecules to hot spots and prevent them from leaving has not been thoroughly considered and studied. Here, a composite MoS2/Ag NP nanopocket detector composed of MoS2 covered with a Ag NP film was fabricated to develop a general SERS method for actively capturing target molecules into hotspots. A finite element method (FEM) simulation of the multiphysics model was used to analyze the distributions of electric field enhancements and hydrodynamic processes in solution and air of the MoS2/Ag NP nanopocket. The results revealed that covering MoS2 slowed the evaporation of the solution, extended the window period for SERS detection, and enhanced the electric field in comparison with the monolayer Ag NP film. Therefore, in the process of dynamic detection, the MoS2/Ag NP nanopocket can provide an efficient and stable signal within 8 min, increasing the high sensitivity and long-term stability of the SERS method. Furthermore, a MoS2/Ag NP nanopocket detector was applied to detect antitumor drugs and monitor hypoxanthine structural changes in serum, which demonstrated long-term stability and high sensitivity for SERS analysis. This MoS2/Ag NP nanopocket detector paves the way for developing the SERS method in various fields.
RESUMEN
Acute kidney injury (AKI) is the main obstacle that limits the use of cisplatin in cancer treatment. Proton pump inhibitors (PPIs), the most commonly used class of medications for gastrointestinal complications in cancer patients, have been reported to cause adverse renal events. However, the effect of PPIs on cisplatin-induced AKI remains unclear. Herein, the effect and mechanism of lansoprazole (LPZ), one of the most frequently prescribed PPIs, on cisplatin-induced AKI were investigated in vivo and in vitro. C57BL/6 mice received a single intraperitoneal (i.p.) injection of cisplatin (18 mg/kg) to induce AKI, and LPZ (12.5 or 25 mg/kg) was administered 2 hours prior to cisplatin administration and then once daily for another 2 days via i.p. injection. The results showed that LPZ significantly aggravated the tubular damage and further increased the elevated levels of serum creatinine and blood urea nitrogen induced by cisplatin. However, LPZ did not enhance cisplatin-induced tubular apoptosis, as evidenced by a lack of significant change in mRNA and protein expression of Bax/Bcl-2 ratio and TUNEL staining. Notably, LPZ increased the number of necrotic renal tubular cells compared to that by cisplatin treatment alone, which was further confirmed by the elevated necroptosis-associated protein expression of RIPK1, p-RIPK3 and p-MLKL. Furthermore, LPZ deteriorated cisplatin-induced inflammation, as revealed by the increased mRNA expression of pro-inflammatory factors including, NLRP3, IL-1ß, TNF-α and caspase 1, as well as neutrophil infiltration. Consistently, in in vitro study, LPZ increased HK-2 cell death and enhanced inflammation, compared with cisplatin treatment alone. Collectively, our results demonstrate that LPZ aggravates cisplatin-induced AKI, and necroptosis may be involved in the exacerbation of kidney damage.
