Di(2-ethylhexyl) phthalate mediates oxidative stress and activates p38MAPK/NF-kB to exacerbate diabetes-induced kidney injury in vitro and in vivo models.

Plasticizer di(2-ethylhexyl) phthalate (DEHP) is employed to make polyethylene polymers. Some studies in epidemiology and toxicology have shown that DEHP exposure over an extended period may be hazardous to the body, including nephrotoxicity, and aggravate kidney damage in the context of underlying disease. However, studies on the toxicity of DEHP in diabetes-induced kidney injury have been rarely reported. Using a high-fat diet (HFD) and streptozotocin (STZ, 35 mg/kg)-induced kidney injury in mice exposed to various daily DEHP dosages, we explored the impacts of DEHP on diabetes-induced kidney injury. We discovered that DEHP exposure significantly promoted the renal inflammatory response and oxidative stress in mice, with increased P-p38 and P-p65 protein levels and exacerbated the loss of podocin. The same findings were observed in vitro after stimulation of podocytes with high glucose (30 mmol/L) and exposure to DEHP. Our results suggest that DEHP exacerbates diabetes-induced kidney injury by mediating oxidative stress and activating p38MAPK/NF-κB.

Cuffless blood-pressure estimation method using a heart-rate variability-derived parameter.

OBJECTIVE: Cuffless blood-pressure (BP) estimation has attracted widespread interest owing to its potential for long-term, non-invasive BP monitoring. But it is still impractical in clinical settings, mainly owing to ongoing challenges with respect to accuracy in hypertensive patients. To better estimate the BP, the current study proposes a new cuffless estimation method that includes a sympathetic tone, which has been reported with a varied pattern in hypertensive patients. APPROACH: First, the heart-rate variability of all subjects is investigated, and a new parameter, the heart-rate power spectrum ratio (HPSR), is proposed to indicate BP dynamics under sympathetic regulation. Then, a new BP estimation model is constructed by integrating HPSP with the pulse transit time (PTT) and photoplethysmography intensity ratio. The estimation accuracy is further evaluated by making comparisons with the standard sphygmomanometer BP on 60 subjects (29 hypertensive and 31 normotensive). MAIN RESULTS: A significant increase in HPSR was observed in hypertensive patients compared to normotensive subjects. Of the 60 subjects, the estimation accuracy was 0.73 ± 10.04 mmHg for systolic BP (SBP) and 0.90 ± 7.10 mmHg for diastolic BP (DBP) in hypertensive patients, which is comparable to 0.54 ± 7.52 mmHg for SBP and 0.82 ± 6.20 mmHg for DBP in normotensive subjects. Furthermore, the proposed method overperformed the traditional PTT-based algorithm by reducing the 3 mmHg error in the standard deviation in hypertensive patients. SIGNIFICANCE: The results of the current study demonstrate that the inclusion of factors associated with autonomic activities in the BP estimation model would improve the BP estimation accuracy, especially for hypertensive subjects.