Design, synthesis and biological evaluation of buthutin derivatives as cardioprotective agents.

Natural products are the important sources in cardiovascular drug development. In this study, twenty-nine buthutin derivatives were designed, synthesized, and evaluated for their NHE-1 inhibition and protective effects on cardiomyocyte injury. The structure of the newly synthesized compounds had been confirmed by H-NMR, C-NMR, and HR-ESI-MS spectra.

YQFM alleviated cardiac hypertrophy by apoptosis inhibition and autophagy regulation via PIK/AKT/mTOR pathway.

Ethnopharmacological Relevance: As a traditional compound preparation of Chinese medicine, Yiqi Fumai lyophilized injection (YQFM) has protective effects on various cardiac diseases including cardiac hypertrophy, which is the primary cause of arrhythmia. However, the involved mechanism remains unclear.

Aim Of The Study: This study was projected to investigate whether YQFM could prevent cardiac hypertrophy and arrhythmia concurrence.

Doxorubicin nanomedicine based on ginsenoside Rg1 with alleviated cardiotoxicity and enhanced antitumor activity.

The authors aimed to develop Dox@Rg1 nanoparticles with decreased cardiotoxicity to expand their application in cancer. Dox@Rg1 nanoparticles were developed by encapsulating doxorubicin (Dox) in a self-assembled Rg1. The antitumor effect of the nanoparticles was estimated using 4T1 tumor-bearing mice and the protective effect on the heart was investigated and .

Specific protein kinase C isoform exerts chronic inhibition on the slowly activating delayed-rectifier potassium current by affecting channel trafficking.

The slowly activating delayed rectifier K current () plays a key role in the repolarization of ventricular action potential in the human heart and is formed by the pore-forming α-subunit encoded by KCNQ1 (Kv7.1) and β-subunit encoded by KCNE1. Evidence suggested that was regulated through protein kinase C (PKC) pathway, but the mechanism is controversial.

Protective effects of rutin on kidney in type 1 diabetic mice.

Diabetic nephropathy is one the most serious diabetic microangiopathies, which is the main cause of mortality in diabetic patients. Our research investigated the protective effects of rutin on kidney of the type 1 diabetes mice induced by streptozotocin (STZ). The levels of kidney weight index (KWI), postprandial plasma glucose (PPG), creatinine (Cre), blood urine nitrogen (BUN), the activity of super oxide dismutase (SOD), malondialdehyde (MDA) and glutathione per oxidase (GSH-Px) were all measured.

Effects of D-Chiro-Inositol on Glucose Metabolism in db/db Mice and the Associated Underlying Mechanisms.

In this study, we observed the effect of D-chiro-inositol (DCI) on glucose consumption in type 2 diabetic db/db mice, and investigated the relevant mechanism. We discovered that the stability of 24-h blood glucose under the nonfasting condition and decreased glucose tolerance were both alleviated after treatment with DCI. Moreover, the content of glycosylated protein and advanced glycation end products in the serum was reduced, the damage in the liver tissue was alleviated, and the synthesis of liver glycogen was significantly promoted.

[Effects of Rutin on Myocardial Enzyme and Cardiac Morphology in Diabetic Mice].

Objective: To study the effects of rutin on myocardial enzyme in serum and myocardial morphology in diabetic mice induced by streptozotocin (STZ).

Methods: A model of type 1 diabetic mice was established in 48 male kunming mice with daily intraperitoneal injection of streptozotocin (STZ) 62.5 mg/kg for 5 consecutive days.

Protective effects of rutin on liver injury in type 2 diabetic db/db mice.

The aim of this study was to evaluate the protective effect of rutin on the liver of type 2 diabetic mice and explore the correlation mechanism. The db/db mice, selected as the type 2 diabetes mellitus (T2DM) models, have random blood glucose (RBG) and glucose level after 2 h of oral glucose loading of more than 16.7 mmol/L.

Protein kinase C epsilon mediates the inhibition of angiotensin II on the slowly activating delayed-rectifier potassium current through channel phosphorylation.

The slowly activating delayed rectifier K current (I) is one of the main repolarizing currents in the human heart. Evidence has shown that angiotensin II (Ang II) regulates I through the protein kinase C (PKC) pathway, but the related results are controversial. This study was designed to identify PKC isoenzymes involved in the regulation of I by Ang II and the underlying molecular mechanism.

Imaging of reactive oxygen species burst from mitochondria using laser scanning confocal microscopy.

Objective: Although several methods have been used to detect the intracellular reactive oxygen species (ROS) generation, it is still difficult to determine where ROS generate from. This study aimed to demonstrate whether ROS generate from mitochondria during oxidative stress induced mitochondria damage in cardiac H9c2 cells by laser scanning confocal microscopy (LSCM).

Methods: Cardiac H9c2 cells were exposed to H2 O2 (1200μM) to induce mitochondrial oxidant damage.

The paradox of dopamine and angiotensin II-mediated Na(+), K(+)-ATPase regulation in renal proximal tubules.

Accumulated studies reported that the natruretic dopamine (DA) and the anti-natruretic angiotensin II (Ang II) represent an important mechanism to regulate renal Na(+) and water excretion through intracellular secondary messengers to inhibit or activate renal proximal tubule (PT) Na(+), K(+)-ATPase (NKA). The antagonistic actions were mediated by the phosphorylation of different position of NKA α₁-subunit and different Pals-associated tight junction protein (PATJ) PDZ domains, the different protein kinase C (PKC) isoforms (PKC-β, PKC-ζ), the common adenylyl cyclase (AC) pathway, and the crosstalk and balance between DA and Ang II to NKA regulation. Besides, Ang II-mediated NKA modulation has bi-phasic effects.