Objective To investigate the serum level of placental growth factor (PLGF) and explore its relationship with left ventricular structure and function in chronic kidney disease (CKD) patients.Methods Seventy-two non-dialysis CKD patients and sixteen age-and sex-matched healthy controls were included in this study.Serum PLGF level was measured by ELISA.Cardiac structure and function were assessed by two dimensional echocardiography.Results (1)The serum level of PLGF in CKD patients[3.32(2.97,19.77) ng/L] was significantly higher compared to the healthy controls [2.33(2.27,2.49) ng/L] (P ＜ 0.01).It progressively increased with the decline of renal function (P＜ 0.05/6).(2)The interventricular septum (IVS),left ventricular posterior wall (LVPW) was significantly higher while the ejection fraction was significantly lower in CKD patients.(3)The serum PLGF level was higher in patients with left ventricular hypertrophy (LVH) than those without LVH [19.05(3.31,21.05) ng/L vs 2.99(2.60,3.32) ng/L,P ＜ 0.05].The prevalence of LVH in the group above median PLGF level was significantly higher than that in the group below the median PLGF level (70％ vs 18％,P ＜ 0.01).(4)PLGF level was positively correlated with left ventricular mass index (LVMI),systolic pressure,diastolic pressure,24 h urine protein,Scr,UA,BUN,iPTH,the history of high blood pressure and was negatively correlated with LVEF,hemoglobin,albumin,eGFR (P ＜ 0.05).Multiple regression results showed that UA,Scr,LVEF,Hb were associated with PLGF level independently (P ＜ 0.01).Conclusions CKD patients have elevated level of PLGF.It has a relationship with cardiac structure and function.It may participate in the occurrence of cardiovascular events.

Objective To investigate the effect and underlying mechanism of Qingguang’an Granules (青光安颗粒剂, QGAG) on mitochondrial autophagy (mitophagy) of retinal ganglion cells (RGCs) in rats with chronic ocular hypertension (COH). Methods Sixty Sprague Dawley (SD) rats, half males and half females, were randomly assigned to three groups: the control, model, and QGAG (2.5 g/kg) groups, with 20 rats in each group. Rats’ model of COH was established by cauterizing episcleral veins in the model group and QGAG group. Three weeks after successful modeling, rats in the QGAG group were intragastrically administered with QGAG, while rats in the control group and the model group received an equal dose of normal saline. After three months of intragastric administration, intraocular pressure (IOP) of all rats was measured. The mitophagy was monitored by the immunofluorescence method, the mitochondrial membrane potential was measured using the JC-1 method, and the morphological changes of mitophagy in RGCs were observed by transmission electron microscopy. Meanwhile, rat RGCs were labeled using the fluorescent gold method, and RGCs density in each group was calculated. Moreover, RGCs apoptosis was observed by TdT-mediated dUTP Nick-End Labeling (TUNEL) assay. Finally, the expression levels of Parkin, optineurin, microtubule-associated protein 1 light chain 3-II/microtubule-associated protein 1 light chain 3-I (LC3-II/LC3-I), recombinant lysosomal associated membrane protein 1 (LAMP1), and B-cell lymphoma-2 (Bcl-2) in RGCs were determined by Western blot assay. The corresponding mRNAs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). Results The QGAG reduced IOP in COH rats, and inhibited mitophagy and apoptosis of RGCs (P < 0.05). Besides, the QGAG significantly increased the expression levels of Parkin and Bcl-2 (P < 0.05), and inhibited the expression levels of optineurin, LAMP1, and LC3-II/LC3-I (P < 0.05) in RGCs of COH rats. Conclusion The QGAG can inhibit mitophagy in RGCs of COH rats and show a protective effect against optic nerve damage caused by glaucoma, which may be mediated through the mitophagy ubiquitination via the Parkin/PINK1-related pathway.