[Construction of an enteritis chip model based on microfluidic technology and its application in the evaluation of nanodrug efficacy].

To simulate the intestinal microenvironment and physiological structure, this study constructed the enteritis chip model via the microfluidic technology. Meanwhile, the Aloe vera polysaccharide copolymer (LDG@AMI) loaded with 5-aminosalicylic acid (5-AMI), the nanodrug LDG@AMI was synthesized, and its anti-inflammatory effects were evaluated through the enteritis chip model. In this study, a fluorescence microscopy was employed to measure the growth conditions of cells and the expression of intestinal barrier protein (ZO-1) and intestinal mucosa protein (WGA) in the enteritis chip. In addition, the morphology, size, and composition of LDG@AMI were measured via a transmission electron microscope, a nanoparticle size analyzer, and a Fourier-transform infrared (FT-IR) spectrometer, respectively. Subsequently, the swelling and drug release properties of LDG@AMI were evaluated by ultraviolet-visible (UV-Vis) spectroscopy. Furthermore, ELISA kits were used to quantify the levels of inflammatory factors including tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1 β (IL-1β) in the enteritis chip. The results indicated that the intestine chip cells exhibited good viability and normal expression of ZO-1, which implied the formation of intestinal barrier. After the treatment with sodium dextran sulfate (DSS), the chip showcased increased permeability, elevated expression level of hypoxia inducible factor-1α (HIF-1α), and significantly declined expression levels of ZO-1 and WGA, which suggested that the enteritis chip model was successfully constructed. LDG@AMI had a particle size of about 80 nm, a high swelling rate, and sustained release properties, accurately responding to the intestinal microenvironment. The LDG@AMI-treated enteritis chip showed higher expression levels of ZO-1 and WGA than the 5-AMI-treated group, which indicated that LDG@AMI possessed the excellent ability of repairing barriers. Compared with those in the normal intestine chip, the expression levels of TNF-α, IL-1β, and IL-6 in the enteritis chip significantly increased, further confirming that the enteritis chip model was successfully constructed. Interestingly, the LDG@AMI-treated enteritis chip showed the lower levels of TNF-α, IL-1β, and IL-6 than the untreated enteritis chip, which verified that LDG@AMI possessed excellent therapeutic effect on enteritis. We successfully construct a microfluidic technology-based enteritis chip model and further evaluate the anti-inflammatory effect of LDG@AMI, expanding new horizons for precise treatment of enteritis.