Biology subjects

Yu, B.-X.

Publications and source records attributed to Yu, B.-X..

2 recordsLinked to original sources

bioRxiv2022

Hydroxycitric acid inhibits oxalate nephropathies formation through crystallization regulation and activation of the PPARα pathway

Oxalate-induced nephropathies comprise a range of kidney disorders, for which there are no efficient pharmacological treatments. Hydroxycitric acid (HCA) is a derivative of citric acid with a variety of pharmacological activities including reducing body weight and calcium salt deposition. However, the specific mechanism of inhibition of oxalate nephropathies by this compound is not well understood. In this study, we successfully applied bioinformatics-based and simulated drug molecular docking approaches to predict potential targets of HCA. Subsequently, we explored the molecular mechanisms of HCA inhibition of renal calcium oxalate (CaOx) deposition and nephrotoxicity in an oxalate-induced NRK-52E cell model and an oxalate nephropathy rat model. HCA could effectively inhibit CaOx crystal deposition and reduce crystal adhesion and oxidative damage, effectively inhibit lipid deposition caused by high oxalate, and reduce lipid nephrotoxicity. HCA is more effective than traditional stone medications in inhibiting CaOx deposition and kidney damage. Further cellular transcriptomic analysis and in vitro results showed that HCA could stably bind peroxisome proliferator-activated receptor (PPAR) and promote PPAR-RXR heterodimer formation, thus promoting the expression of downstream oxidative stress molecules (Nrf2, HO-1, SOD) and inhibiting calcium ion release and mitochondrial dysfunction, thus reducing oxalate-induced renal lipid peroxidation damage. Therefore, HCA, a novel drug with the ability to modulate lipid metabolism and inhibit CaOx formation, may be a therapeutic option for the treatment of oxalate nephropathies.

biochemistry↗

bioRxiv2019

Inland-coastal bifurcation of southern East Asians revealed by Hmong-Mien genomic history

The early history of the Hmong-Mien language family and its speakers is elusive. A good variety of Hmong-Mien-speaking groups distribute in Central China. Here, we report 903 high-resolution Y-chromosomal, 624 full-sequencing mitochondrial, and 415 autosomal samples from 20 populations in Central China, mainly Hunan Province. We identify an autosomal component which is commonly seen in all the Hmong-Mien-speaking populations, with nearly unmixed composition in Pahng. In contrast, Hmong and Mien respectively demonstrate additional genomic affinity to Tibeto-Burman and Kra-Dai speakers. We also discover two prevalent uniparental lineages of Hmong-Mien speakers. Y-chromosomal haplogroup O2a2a1b1a1b-N5 diverged [~]2,330 years before present (BP), approximately coinciding with the estimated time of Proto-Hmong-Mien ([~]2,500 BP), whereas mitochondrial haplogroup B5a1c1a significantly correlates with Pahng and Mien. All the evidence indicates a founding population substantially contributing to present-day Hmong-Mien speakers. Consistent with the two distinct routes of agricultural expansion from southern China, this Hmong-Mien founding ancestry is phylogenetically closer to the founding ancestry of Neolithic Mainland Southeast Asians and present-day isolated Austroasiatic-speaking populations than Austronesians. The spatial and temporal distribution of the southern East Asian lineage is also compatible with the scenario of out-of-southern-China farming dispersal. Thus, our finding reveals an inland-coastal genetic discrepancy related to the farming pioneers in southern China and supports an inland southern China origin of an ancestral meta-population contributing to both Hmong-Mien and Austroasiatic speakers.

genetics↗