<p><em>Advanced glycation end products (AGE) are amalgamated in the development of certain pathophysiologies including diabetic retinopathy (DR). Procyanidin-B2 (PCB2), an active principle of cinnamon, has shown to inhibit AGE formation</em><em>. In current study we inspected the protective role of PCB2 to prevent DR in diabetic rats.<strong> </strong>Diabetes was induced in Wistar-NIN rats by intraperitoneal injection of streptozotocin (35 mg/kg bodyweight) and the control rats received vehicle alone. The retinal morphology was studied by microscopy and immunohistochemistry of diabetic and control rats. The expression of retinal selective genes analysis was done via real-time PCR. Immunoblotting of diabetic and control rat retina was studied. Gene expression and immunohistochemistry and immunofluorescence analysis of diabetic retina from PCB2 and cinnamon fed rat showed declined expression of VEGF and GFAP and increased expression of NGF. Immunoblotting analysis resulted that feeding of PCB2 significantly reserved the formation of carboxy methyl lysine and RAGE in diabetic rats compare with controls. The results indicate that PCB2 was effective in protecting the diabetic retina from development of diabetic retinopathy in rats owing to its antiglycating potential. Thus, active principle of dietary sources, such as PCB2, may be explored for the prevention or delay of DR.<strong></strong></em></p>
Diabetic kidney disease (DKD) is the primary cause of chronic kidney disease (CKD) worldwide. Altered mineral levels leading to adverse outcomes are widely reported in diabetes, but studies regarding their status in DKD are limited. To explore the status of minerals, a hospital-based case-control study was taken up with 54 healthy controls (C) and 140 subjects with type 2 diabetes wherein 74 subjects with diabetes, and CKD formed the DKD group, and 66 subjects with diabetes, no CKD formed the DNCKD group. High-resolution inductively coupled plasma mass spectrometry was used to evaluate the blood levels of minerals (Ca, V, Cr, Mn, Fe, Co, Cu, Zn, and Se), and raw food-based food frequency questionnaire for dietary intakes. The median values of plasma Ca in the DKD group were significantly lower compared with the DNCKD and C groups (10.5 mg/dL vs. 11.0 mg/dL and 11.7 mg/dL, p < 0.001). Furthermore, plasma Ca levels lowered with declining kidney function, as evidenced by the estimated glomerular filtration rate (eGFR) and albuminuria segregation. Dietary intake of minerals did not correlate with the corresponding plasma levels. However, in the DKD group, eGFR correlated positively with the plasma levels of Ca (r = 0.422, p = 0.001), Cr (r = 0.351, p = 0.008), Mn (r = 0.338, p = 0.011), Fe (r = 0.403, p = 0.002), Cu (r = 0.274, p = 0.041) and negatively with Se (r= -0.486, p < 0.001). Plasma Ca levels are lower in the DKD group with a strong positive association with eGFR, indicating its role in predicting the onset and progression of kidney function decline.
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Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness (AHR), inflammation, and goblet cell hyperplasia. Both Th1 and Th2 cytokines, including IFN-γ, IL-4, and IL-13 have been shown to induce asthma; however, the underlying mechanisms remain unclear. We observed a significant increase in the expression of IL-31RA, but not its cognate ligand IL-31 during house dust mite- and Schistosoma mansoni soluble egg antigen-induced allergic asthma. In support of this, IFN-γ and Th2 cytokines, IL-4 and IL-13, upregulated IL-31RA but not IL-31 in airway smooth muscle cells (ASMC). Importantly, the loss of IL-31RA attenuated AHR but had no effects on inflammation and goblet cell hyperplasia in allergic asthma or mice treated with IL-13 or IFNγ. Mechanistically, we demonstrate that IL-31RA functions as a positive regulator of muscarinic acetylcholine receptor 3 (CHRM3) expression and calcium signaling involved in the contractility of ASMC. Together, these results identified a novel role for IL-31RA in ASMC contractility and AHR distinct from airway inflammation and goblet cell hyperplasia in asthma.
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