Brassica rapa Polysaccharides Ameliorate CCl4‐Induced Acute Liver Injury in Mice through Inhibiting Inflammatory Apoptotic Response and Oxidative Stress

Brassica rapa L., also called NIUMA, is used empirically in Tibetan medicine for its antioxidant, anti‐inflammatory and antiradiation activities. This study explored the hepatoprotective effects of B. rapa polysaccharides (BRPs) on acute liver injury induced by carbon tetrachloride (CCl₄) in mice and the underlying mechanisms. Mice were treated with CCl₄ after the oral administration of BRPs (55, 110 and 220 mg/kg) or bifendate (100 mg/kg) for 7 days. Blood and liver samples of mice were collected for analysis after 24 h. The ALP, ALT and AST levels and the biological activities of SOD, MDA and GSH?Px were measured. Histopathological changes in the liver were determined through hematoxylin and eosin staining. Moreover, TNF‐α, IL‐1β and IL‐6 expression levels were detected by commercial reagent kits. Finally, Western blot analysis was used to check the relative expression levels of caspase‐3, p‐JAK2 and p‐STAT3. The BRP pre‐treatment significantly decreased the enzymatic activities of ALT, ALP and AST in the serum, markedly increased the activities of SOD and GSH?Px in the liver and reduced the MDA concentration in the liver. BRPs alleviated hepatocyte injury and markedly inhibited the expression of TNF‐α, IL‐1β and IL‐6, also downregulating the CCl₄‐induced hepatic tissue expression of caspase‐3. Furthermore, BRPs inhibited the JAK2/STAT3 signaling pathway in a dose‐dependent manner in the liver. This study demonstrated that BRPs exert hepatoprotective effect against the CCl₄‐induced liver injury via modulating the apoptotic and inflammatory responses and downregulating the JAK2/STAT3 signaling pathway. Therefore, B. rapa could be considered a hepatoprotective medicine.     

Soil seed bank in different vegetation types in the Loess Plateau region and its role in vegetation restoration

In the Loess Plateau region, soil erosion is a serious problem. Vegetation restoration is an effective approach to control soil erosion and improve ecosystems. The soil seed bank generally plays an important role in vegetation restoration after disturbance. Thus, we reviewed soil seed bank studies to reveal the soil seed bank characteristics and its role in vegetation restoration in three vegetation types (forest, forest‐steppe, and steppe). We selected 38 seed bank studies and analyzed several seed bank characteristics, such as seed density, species composition, and the relationship between seed size and seed bank. We also assessed the role of the soil seed bank in vegetation restoration. The soil seed bank density ranged from 2,331 ± 1,993 to 6,985 ± 4,047 seeds/m² among the different vegetation types. In the soil seed bank, perennial herbs and grasses accounted for 51.5% of the total species. Native species that were dominant or common in the standing vegetation usually had relatively high seed bank densities. Moreover, species with smaller seeds generally had higher soil seed bank densities. The present study indicates that the soil seed bank plays a significant role in spontaneous vegetation restoration, especially during the early successional stages in abandoned slope farmlands and grazing‐excluded grasslands. However, species with large seeds or transient soil seed banks should be reintroduced through seeding to accelerate target species restoration. More studies on soil seed banks need to be conducted to comprehensively reveal their characteristics.     

LINC00667 promotes Wilms’ tumor metastasis and stemness by sponging miR‐200b/c/429 family to regulate IKK‐β

Wilms' tumor, also known as nephroblastoma, is a kind of pediatric renal cancer. Previous studies have indicated that microRNAs (miRNAs) regulate various cancers progression. However, whether miR‐200 family regulated Wilms' tumor progression remains to be elucidated. In our study, miR‐200b/c/429 expression was downregulated in Wilms' tumor tissue samples from 25 patients. And data from three independent analyses of quantitative real‐time polymerase chain reaction revealed that the expression of miR‐200b/c/429 was downregulated in Wilms' tumor cell lines. Functionally, Cell counting kit‐8 assay revealed that cell viability was reduced by overexpressing miR‐200b/c/429. Transwell assay manifested that cell migration and invasion was hindered by miR‐200b/c/429 overexpression. Sphere‐forming and western blot assays demonstrated that miR‐200b/c/429 overexpression suppressed the sphere formation ability. Mechanically, nuclear factor‐κB (NF‐κB) pathway was confirmed to be associated with Wilms' tumor progression; miR‐200b/c/429 overexpression inactivated NF‐κB pathway as miR‐200b/c/429 was identified to target IκB kinase β (IKK‐β), an NF‐κB pathway‐related gene. Moreover, miR‐200b/c/429 was sponged by LINC00667 in Wilms' tumor cells. LINC00667 competitively bound with miR‐200b/c/429 to regulate IKK‐β expression and then activated NF‐κB pathway in Wilms' tumor. Subsequently, rescue assays illustrated that silencing of IKK‐β could reverse the effect of miR‐200b/c/429 inhibition on the progression of sh‐LINC00667‐transfected Wilms' tumor cells. In summary, LINC00667 promoted Wilms' tumor progression by sponging miR‐200b/c/429 family to regulate IKK‐β.     

番茄转录因子基因SlWRKY6的克隆与原核表达分析

该研究基于番茄基因组数据库SGN(Sol Genomic Network)信息,利用RT PCR从栽培番茄‘M82’(Solanum lycopersicum)中成功克隆到番茄SlWRKY6基因(登录号：Solyc02g080890),通过qRT PCR方法和原核表达初步验证其生物学功能。结果表明：(1)生物信息学分析显示,番茄SlWRKY6基因ORF全长1 653 bp,编码550个氨基酸,其蛋白结构含有1个WRKYGQK保守结构域和C₂H₂锌指结构域,属于IIb类;其基因启动子上游1 500 bp含有多个激素响应元件和非生物胁迫响应元件。(2)进化树分析显示,SlWRKY6与潘那利番茄SpWRKY31 X1(NP_001352691.1)的相似性最高,且定位于细胞核内。(3)qRT PCR结果显示,SlWRKY6基因在番茄根、茎、叶中均有表达,在叶中的表达量最高,且受盐和干旱诱导表达。(4)SDS PAGE及Western blot结果显示,pET 30a SlWRKY6重组蛋白的大小约66 kDa,与预期大小一致。(5)原核表达分析显示,重组菌E. coli BL21∷pET 30a SlWRKY6在不同浓度盐(NaCl)和干旱(Mannitol)胁迫下生长速度显著低于对照菌E. coli BL21∷pET 30a,且在400 mmol/L NaCl、800 mmol/L甘露醇胁迫条件下最为显著;滴板实验初步验证SlWRKY6转录因子能提高重组菌E. coli BL21∷pET 30a SlWRKY6在ABA和pH 9(NaOH)胁迫的耐受性;在400 mmol/L NaCl、pH 5(HCl)、800 mmol/L甘露醇胁迫条件下耐受能力降低。研究表明,SlWRKY6转录因子可能通过参与ABA途径来响应非生物胁迫。     

Role of TRPV4-P2X7 Pathway in Neuropathic Pain in Rats with Chronic Compression of the Dorsal Root Ganglion

Neurochemical Research - Transient receptor potential vanilloid 4 (TRPV4) is a Ca2+-permeable non-selective cation channel that is involved in the development of neuropathic pain. P2X7 receptor...     

Characterizing the impacts of highway pavement in a newly planned greater bay area economic belt in China

The International Journal of Life Cycle Assessment - As an ambitious strategy of national interest in China and with an aim at achieving the ‘one-hour economic circle’ among Greater Bay...     

Slc20a1b is essential for hematopoietic stem/progenitor cell expansion in zebrafish

Science China Life Sciences - Hematopoietic stem and progenitor cells (HSPCs) are able to self-renew and can give rise to all blood lineages throughout their lifetime, yet the mechanisms regulating...     

Evaluation of the efficacy and safety of hydroxychloroquine in comparison with chloroquine in moderate and severe patients with COVID-19

Science China Life Sciences -     

ARL4C might serve as a prognostic factor and a novel therapeutic target for gastric cancer: bioinformatics analyses and biological experiments

The ADP-ribosylation factor-like proteins (ARLs) have been proved to regulate the malignant phenotypes of several cancers. However, the exact role of ARLs in gastric cancer (GC) remains elusive. In this study, we systematically investigate the expression status, interactive relations, potential pathways, genetic variations and clinical values of ARLs in GC. We find that ARLs are significantly dysregulated in GC and involved in various cancer-related pathways. Subsequently, machine learning models identify ARL4C as one of the two most significant clinical indicators among ARLs for GC. Furthermore, ARL4C silencing remarkably inhibits the growth and metastasis of GC cells both in vitro and in vivo. Moreover, enrichment analysis indicates that ARL4C is highly correlated with TGF-β1 signalling. Correspondingly, TGF-β1 treatment dramatically increases ARL4C expression and ARL4C knockdown inhibits the phosphorylation level of Smads, downstream factors of TGF-β1. Meanwhile, the coexpression of ARL4C and TGF-β1 worsens the prognosis of GC patients. Our work comprehensively demonstrates the crucial role of ARLs in the carcinogenesis of GC and the specific mechanisms underlying the GC-promoting effects of TGF-β1. More importantly, we uncover the great promise of ARL4C-targeted therapy in improving the efficacy of TGF-β1 inhibitors for GC patients.