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Background: Puerarin is an isoflavone compound isolated from the roots of a leguminous plant, the wild kudzu. Various functional activities of this compound in multiple diseases have been reported. However, the effect and mechanism of puerarin in improving blood pressure remain non-elucidated. Purpose: The current study was designed to assess the preventive effects of puerarin on the onset and progression of hypertension and to verify the hypothesis that puerarin alleviates blood pressure by inhibiting the ROS/TLR4/NLRP3 inflammasome signaling pathway in the hypothalamic paraventricular nucleus (PVN) of salt-induced prehypertensive rats. Methods: Male Dahl salt-sensitive rats were fed low NaCl salt (3% in drinking water) for the control (NS) group or 8% (HS) to induce prehypertension. Each batch was divided into two group and treated by bilateral PVN microinjection with either artificial cerebrospinal fluid or puerarin through a micro-osmotic pump for 6 weeks. The mean arterial pressure (MAP) was recorded, and samples were collected and analyzed. Results: We concluded that puerarin significantly prevented the elevation of blood pressure and effectively alleviated the increase in heart rate caused by high salt. Norepinephrine (NE) in the plasma of salt-induced prehypertensive rats also decreased upon puerarin chronic infusion. Additionally, analysis of the PVN sample revealed that puerarin pretreatment decreased the positive cells and gene level of TLR4 (Toll-like receptor 4), NLRP3, Caspase-1 p10, NOX2, MyD88, NOX4, and proinflammatory cytokines in the PVN. Puerarin pretreatment also decreased NF-κBp65 activity, inhibited oxidative stress, and alleviated inflammatory responses in the PVN. Conclusion: We conclude that puerarin alleviated blood pressure via inhibition of the ROS/TLR4/NLRP3 inflammasome signaling pathway in the PVN, suggesting the therapeutic potential of puerarin in the prevention of hypertension. [ABSTRACT FROM AUTHOR]

Based on the transport equation of the semiconductor device model for 0.524 eV GeSn alloy and the experimental parameters of the material, the thermalâ€"electricity conversion performance governed by a GeSn diode has been systematically studied in its normal and inverted structures. For the normal p+/n (n+/p) structure, it is demonstrated here that an optimal base doping N d(a) = 3 (7) Ă— 1018 cmâˆ'3 is observed, and the superior p+/n structure can achieve a higher performance. To reduce material consumption, an economical active layer can comprise a 100 nmâ€"300 nm emitter and a 3 ÎĽmâ€"6 ÎĽm base to attain comparable performance to that for the optimal configuration. Our results offer many useful guidelines for the fabrication of economical GeSn thermophotovoltaic devices. [ABSTRACT FROM AUTHOR]

Background: Inflammation and oxidative stress play important roles in energy imbalance and its complications. Recent research indicates that hypothalamic inflammation may contribute to the pathogenesis of metabolic syndrome and cardiac dysfunction, but the mechanisms remain unclear. We hypothesized that suppression of the proinflammatory IKKβ/NF-κB pathway in the hypothalamus can improve energy balance and cardiac function in type 2 diabetic (T2D) rats. Methods: Normal and T2D rats received bilateral hypothalamic arcuate nucleus (ARC) infusions of the IKKβ inhibitor SC-514 or vehicle via osmotic minipump. Metabolic phenotyping, immunohistochemical analyses, and biochemical analyses were used to investigate the outcomes of inhibition of the hypothalamic IKKβ. Echocardiography and glucometer were used for measuring cardiac function and blood glucose, respectively. Blood samples were collected for the evaluation of circulating proinflammatory cytokines. Heart was harvested for cardiac morphology evaluations. The ARC was harvested and analyzed for IKKβ, NF-κB, proinflammatory cytokines, reactive oxygen species (ROS), and NAD(P)H (gp91phox, p47phox) oxidase activity levels and neuropeptides. Results: Compared with normal rats, T2D rats were characterized by hyperglycemia, hyperinsulinemia, glucose intolerance, cardiac dysfunction, as well as higher ARC levels of IKKβ, NF-κB, proinflammatory cytokines, ROS, gp91phox, and p47phox. ARC infusion of the IKKβ inhibitor SC-514 attenuated all these changes in T2D rats, but not in normal rats. Conclusions: Our results indicate that the hypothalamic IKKβ/NF-κB pathway plays a key role in modulating energy imbalance and cardiac dysfunction, suggesting its potential therapeutic role during type 2 diabetes mellitus. [ABSTRACT FROM AUTHOR]

A novel Co(II)-containing metal–organic framework [Co3(OH)2(H2TCPP)2](DMF)3 (1) based on a linear trinuclear Co(II) cluster-based unit has been successfully prepared by using a nanosized tetracarboxylate ligand 2,3,5,6-tetrakis(4-carboxyphenyl)pyrazine (H4TCPP) as the organic building block under the solvothermal reaction. Gas adsorption studies reveal that the mixtures of C2H2/CH4 and C2H2/CO2 could be selectively separated by the obtained resulting solvent free 1 (denoted as 1a hereafter). To deep evaluate the protective function of complex for acute glomerulonephritis (AGN) disease in vitro, the following experiments were conducted. (a) Real time Reverse transcription-Polymerase Chain Reaction (RT-PCR) was carried out to determine the relative expression of Nuclear factor kappa beta (nf-κb) and Tumor Necrosis Factor-α (tnf-α) in the glomerulus cells after bacterial infection along with complex 1 treatment. (b) The enzyme linked immunosorbent assay (ELISA) was conducted to determine the IL-1β and IL-6 released by glomerular cells after complex 1 treatment. (c) The results obtained through molecular docking exhibited possible regulation mechanism on the binding affinity between compound 1 and target protein. [ABSTRACT FROM AUTHOR]