National Health and Family Planning Commission

About: National Health and Family Planning Commission is a government organization based out in Beijing, China. It is known for research contribution in the topics: Population & Kashin–Beck disease. The organization has 2379 authors who have published 1440 publications receiving 20078 citations. The organization is also known as: Ministry of Health of the People's Republic of China.

The Effect of Velvet Antler Proteins on Cardiac Microvascular Endothelial Cells Challenged with Ischemia-Hypoxia.

Abstract: Velvet antler (VA) is a precious traditional Chinese medicine that is capable of repeated regeneration. Based on the Chinese medicine theory of coordination the heart and kidneys, VA has been employed to treat heart diseases, including ischemic heart disease, heart failure, and arrhythmia. We examined the effects of VA proteins on primary cardiac microvascular endothelial cells (CMECs) that were subjected to ischemia-hypoxia (IH) to investigate their effects on and mechanism of action in the treatment of ischemic heart disease. Velvet antler proteins (VA-pro) were extracted with water as the solvent, the ultrasonic wave method, and freeze-drying technology; then it was analyzed by Nano LC-MS/MS. In addition, the role of VA-pro in cell viability, proliferation, apoptosis, and mitochondrial membrane potential (MMP) were evaluated by the CCK8 assay, the EdU assay, the Annexin V-FITC/PI double-staining assay, and the JC-1 assay, respectively. Cell migration were evaluated by the scratch assay and the Transwell assay. The expression of apoptosis-associate proteins, Akt and p-Akt, and tube formation in Matrigel of CMECs were also detected. In total, 386 VA-pro were identified. Our results showed that IH significantly reduced the viability of the CMECs and suppressed copies of DNA to hold back CMEC proliferation, and it decreased the migration of CMECs, tubule formation ability, and MMP. VA-pro treatment resulted in an improvement in CMECs’ viability, proliferation, migration, and tubule formation ability as well as retaining the stability of MMP. Severe apoptosis was induced after CMECs were cultured in IH conditions, while VA-pro decreased the number of apoptotic cells. Similarly, the expression of pro-apoptosis proteins was higher, but the expression of anti-apoptosis proteins was lower in the IH group; VA-pro reversed these changes. These findings suggest that VA-pro ameliorate CMEC injuries induced by IH via regulating the PI3K/Akt signaling pathway.

Cyanidin-3-O-glucoside attenuates endothelial cell dysfunction by modulating miR-204-5p/SIRT1-mediated inflammation and apoptosis.

Abstract: Endothelial cell (EC) dysfunction is a major symptom associated with the initiation of atherosclerosis (AS) Cyanidin-3-O-glucoside (C3G) has the potentials to attenuate AS symptoms In the current study, the mechanism driving the effects of C3G on AS rabbits and injured ECs were explored by focusing on the changes in miR-204-5p/SIRT1 axis AS symptoms were induced in rabbits using high-fatty diet (HFD) plus balloon catheter injured method and handled with C3G of two doses Then the changes in artery wall structure, hemodynamics parameters, blood lipid level, systemic inflammation, and miR-204-5p/SIRT1 axis were detected EC dysfunction was imitated by subjecting human umbilical vein endothelial cells (HUVECs) to TNF-α, which was then handled with C3G The changes in apoptosis, inflammation, and miR-204-5p/SIRT1 axis were detected The results showed that the administrations of C3G improved artery wall structure and hemodynamics parameters, decreased blood lipid levels, and suppressed pro-inflammatory cytokine production in HFD rabbits, which was associated with the down-regulation of miR-204-5p and the up-regulation of SIRT1 In in vitro assays, the treatments of C3G suppressed apoptosis, inhibited inflammation, down-regulated miR-204-5p level, and induced SIRT1 level in HUVECs The overexpression of miR-204-5p impaired the protective effects of C3G on the injured HUVECs by increasing cell apoptosis and inflammation The findings outlined in the current study confirmed the protective effects of C3G on EC function, which was associated with the down-regulation of miR-204-5p and the up-regulation of SIRT1

Triclosan Suppresses Testicular Steroidogenesis via the miR-6321/JNK/ Nur77 Cascade.

Abstract: Background/aims Triclosan (TCS), a broad-spectrum antibacterial and antifungal compound and an endocrine disruptor, has anti-androgenic properties and could adversely affect male reproduction and fertility. Methods To elucidate the underlying roles of miRNAs and the MAPK pathway in TCS-mediated repression of testicular steroidogenesis, Sprague-Dawley male rats were dosed daily with TCS for 31 days, and TM3 cells were exposed to TCS for 24 h after the pretreatments with the activator of JNK, Nur77 siRNA, or recombinant lentivirus vector for Nur77. Tissues and/or cells were analyzed by several techniques including transmission electron microscopy, lentivirus production, overexpression, gene silencing, luciferase reporter assay, chromatin immunoprecipitation, western blot, and real-time PCR. Results TCS caused histopathologic alterations in the testis and reduced plasma LH and testicular testosterone. TCS induced miR-6321 expression, which in turn depressed its target gene, Map3k1. The inhibition of Map3k1 subsequently inactivated its downstream JNK/c-Jun pathway. ChIP and qPCR assays confirmed that c-Jun directly bound to the Nur77 DNA promoter regions to regulate Nur77 expression. The knockdown and overexpression of Nur77 demonstrated that the JNK/c-Jun-mediated decline in the transcription and translation of Nur77 resulted in the depression of steroidogenic proteins including SRB1, StAR, and 3β-HSD. Intriguingly, the protein expressions of 5α-Reductases (SRD5A1 and SRD5A2) were also downregulated after TCS exposure. Conclusion Taken together, the miR-6321/Map3k1-regulated JNK/c-Jun/ Nur77 cascade contributes to TCS-caused suppression of testicular steroidogenesis, and the decrease in 5α-Reductase expressions may be the compensatory mechanism.

Transcutaneous Electrical Acupoint Stimulation in Early Life Changes Synaptic Plasticity and Improves Symptoms in a Valproic Acid-Induced Rat Model of Autism.

Abstract: Autism spectrum disorder (ASD) is a developmental disorder characterized by social behavior deficit in childhood without satisfactory medical intervention. Transcutaneous electrical acupoint stimulation (TEAS) is a noninvasive technique derived from acupuncture and has been shown to have similar therapeutic effects in many diseases. Valproic acid- (VPA-) induced ASD is a known model of ASD in rats. The therapeutic efficacy of TEAS was evaluated in the VPA model of ASD in the present study. The offspring of a VPA-treated rat received TEAS in the early life stage followed by a series of examinations conducted in their adolescence. The results show that following TEAS treatment in early life, the social and cognitive ability in adolescence of the offspring of a VPA rat were significantly improved. In addition, the abnormal pain threshold was significantly corrected. Additional studies demonstrated that the dendritic spine density of the primary sensory cortex was decreased with Golgi staining. Results of the transcriptomic study showed that expression of some transcription factors such as the neurotrophic factor were downregulated in the hypothalamus of the VPA model of ASD. The reduced gene expression was reversed following TEAS. These results suggest that TEAS in the early life stage may mitigate disorders of social and recognition ability and normalize the pain threshold of the ASD rat model. The mechanism involved may be related to improvement of synaptic plasticity.