ABSTRACT
Objective To investigate the changes in the expression of cold-inducible RNA-binding protein (CIRBP) in a radiation-induced lung injury model. Methods Thirty male C57BL/6 mice were randomly divided by body weight into control group (no intervention) and model group (single chest X-ray irradiation with a dose of 20 Gy to build a radiation-induced lung injury model). The mice were dissected five weeks after irradiation. Hematoxylin-eosin staining and Masson staining were used to observe the pathological changes of the lung tissue and the deposition of collagen fibers. Immunohistochemistry was used to measure the expression of the inflammatory factors interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the lung tissue. qRT-PCR was used to measure the expression of CIRBP mRNA in the lung tissue. The expression of CIRBP protein in the lung tissue was determined by the immunofluorescence assay and Western blot. Results Compared with the control group, the model group showed significant pulmonary vascular congestion, significant inflammatory cell infiltration, significant thickening of some alveolar septa, significantly increased IL-6 expression [(129.41 ± 5.58) vs (187.22 ± 34.77), t = 3.179, P < 0.05], significantly increased TNF-α expression [(137.52 ± 23.53) vs (187.02 ± 19.16), t = 5.069, P < 0.05], significantly increased CIRBP mRNA expression [(1 ± 0.08) vs (1.97 ± 0.39), t = 3.45, P < 0.05], and significantly increased CIRBP protein expression [(9.32 ± 1.26) vs (14.76 ± 1.61), t = 3.751, P < 0.05], by the immunofluorescence assay; [(1.13 ± 0.17) vs (1.49 ± 0.14), t = 2.819, P < 0.05], by Western blot). Conclusion The expression of CIRBP is significantly increased in the radiation-induced lung injury model, which may be an important pro-inflammatory factor in radiation-induced lung injury.
ABSTRACT
The relationship between PEPT1 (peptide transporter) and drug efficacy has drawn more and more attention in the treatment of disease. PEPT1 represents a promising strategy for improvement of drug bioavailability and an important starting point for clinical rationalization of drug selection. The effect of PEPT1 on transport and pharmacokinetics of amoxicillin was investigated under hypoxia condition at high altitude in rat. The mRNA and protein expressions of PEPT1 were increased by 36.87%, 216.21%, 577.8% and 535.9% respectively in the hypoxia group in the small intestine and kidney of rats. However, the mRNA and protein expressions of PEPT1 were reduced by 43.90% and 84.7% in the liver. Compared with the control group, the AUC, tmax, Cmax, MRT and t1/2 of amoxicillin were significantly enhanced by 312.17%, 63.04%, 110.93%, 67.11% and 16.96% respectively in the hypoxia group, while the CL was significantly decreased by 74.51%. After acute exposure to high altitude, the expressions of drug transporter PEPT1 were distinctly changed in rat tissues, which can affect the pharmacokinetics of amoxicillin.
ABSTRACT
OBJECTIVE: To reveal the mRNA expression change of BKCa channel in renal artery in different course in T2DM nephropathy rats. METHODS: T2DM nephropathy models were induced by one side nephrotomy, high-fat diet in rats and small doses of streptozotocin through intraperitoneal injection; Real-time PCR were performed to verify mRNA expression. Then body weight, 24 h urinary albumin, blood urea nitrogen(BUN), serum creatinine(Scr), kidney weight are measured. Renal tissue was observed under optical and electron microscope. RESULTS: Blood glucose, blood insulin, serum creatinine, urea nitrogen, 24 h urinary albumin, kidney hypertrophy index of T2DM nephropathy rats in 8 weeks and 12 weeks, were significantly higher than that of control group (P<0.05, P<0.01);the rat kidney pathological morphological changes were obvious. Compared with the control group, ɑ subunit expression of BKCa in the model group at 8 weeks and 12 weeks were obviously unchanged;β1 subunit expression of BKCa were reduced(P<0.05, P<0.01). CONCLUSION: The mRNA expression of BKCa are reduced in renal artery in different course, and this chang is consistent with the pathological changes degree of kidney in T2DM nephropathy rats.