Paleogeography of the southwestern Ordos Basin and exhumation history of the Liupan Shan area.

The Liupan Shan, situated on the southwestern Ordos Basin, underwent Cenozoic uplift caused by the India-Asia collision and subsequent northeastward tectonic movements. The strata in this region record both the paleogeography of the southwestern Ordos Basin and the uplift history of the Tibetan Plateau. However, past studies have rarely analyzed the strata comprehensively, resulting in overlooked information within them. We present the first detrital zircon (U-Th)/He (ZHe) data from the Lower Cretaceous deposits of the Liupan Shan and the Upper Miocene red clay of Chaona, constraining a maximum burial depth of less than 6-7 km at 60 Ma for the Liupan area. By integrating zircon U-Pb ages, paleocurrent data, and sedimentary facies, we found a primary ZHe age peak (∼210 Ma) indicating that the Lower Cretaceous deposits were sourced from the Qinling Orogenic Belt, while the red clay was likely originated from the Liupan Shan. Although the Chaona strata are not preserved in the Liupan Shan, our results suggest that the Miocene Chaona section is crucial for understanding the Late Cenozoic uplift of the Liupan Shan. The distinct stratigraphic ages and source areas reflect the complex depositional and tectonic history of the region. Thermal modeling results revealed three stages of tectonic events (Late Cretaceous, Late Paleocene-Early Eocene, and Late Cenozoic), which are linked to plate interaction. Our findings offer new insights into the long-term tectonic evolution of the Tibetan Plateau.

Organoboron Polymorphs with Different Molecular Packing Modes for Optical Waveguides.

Organoboron compounds offer a new strategy to design optoelectronic materials with high fluorescence efficiency. In this paper, the organoboron compound B-BNBP with double B←N bridged bipyridine bearing four fluorine atoms as core unit is facilely synthesized and exhibits a narrowband emission spectrum and a high photoluminescence quantum yield (PLQY) of 86.53 % in solution. Its polymorphic crystals were controllable prepared by different solution self-assembly methods. Two microcrystals possess different molecular packing modes, one-dimensional microstrips (1D-MSs) for H-aggregation and two-dimensional microdisks (2D-MDs) for J-aggregation, owing to abundant intermolecular interactions of four fluorine atoms sticking out conjugated plane. Their structure-property relationships were investigated by crystallographic analysis and theoretical calculation. Strong emission spectra with the full width at half maximum (FWHM) of less than 30 nm can also be observed in thin film and 2D-MDs. 1D-MSs possess thermally activated delayed fluorescence (TADF) property and exhibit superior optical waveguide performance with an optical loss of 0.061 dB/µm. This work enriches the diversity of polymorphic microcrystals and further reveals the structure-property relationship in organoboron micro/nano-crystals.

Salvianolic acid B inhibits hepatic stellate cell activation and liver fibrosis by targeting PDGFRß.

Liver fibrosis is a reversible pathological process and a wound healing response to liver injury. As an early stage of various liver diseases, liver fibrosis can develop into cirrhosis, liver failure, and even liver cancer if not controlled in time. Salvia miltiorrhiza is a medicinal plant with hepatoprotective effects. Salvianolic acid B (Sal B) is the representative component of S. miltiorrhiza. Many studies have reported the anti-liver fibrosis effects and mechanisms of Sal B. However, the direct anti-fibrotic targets of Sal B have not yet been reported. Platelet-derived growth factor receptor ß (PDGFRß) is one of the most classical targets in liver fibrosis, which is closely related to hepatic stellate cells (HSCs) activated. Previously, we established and applied a PDGFRß affinity chromatography model, and found that Sal B binds well to PDGFRß. Therefore, this study aimed to investigate the direct targets of Sal B against liver fibrosis. We confirmed the binding ability of Sal B to PDGFRß by molecular docking and a surface plasmon resonance biosensor. Our findings indicated that Sal B targeted PDGFRß to inhibit the activation, migration and proliferation of HSCs and suppressed the PDGF-BB-induced PDGFRß signaling pathway. Annexin V-FITC/PI assay showed that Sal B reversed the PDGF-BB-induced decrease in HSC apoptosis rate. In the mouse liver fibrosis model, Sal B inhibited the PDGFRß signaling pathway, HSC activation and reduced inflammatory response, ultimately improved CCl4-induced liver fibrosis. In summary, the direct anti-fibrotic targets of Sal B may be PDGFRß, and this study clarified the anti-liver fibrosis effects and mechanism of Sal B.

Schizandrin C regulates lipid metabolism and inflammation in liver fibrosis by NF-κB and p38/ERK MAPK signaling pathways.

Liver fibrosis is considered a sustained wound healing response and metabolic syndrome, and its therapy is of great significance for chronic liver disease. Schizandrin C, as one lignan from hepatic protectant Schisandra chinensis, can depress the oxidative effect and lipid peroxidation, and protect against liver injury. In this study, C57BL/6J mice were used to estimate a liver fibrosis model by CCl4, and Schizandrin C exerted an anti-hepatic fibrosis effect, as evidenced by decreased alanine aminotransferase, aspartate aminotransferase and total bilirubin activities in serum, lower hydroxyproline content, recuperative structure and less collagen accumulation in the liver. In addition, Schizandrin C reduced the expressions of alpha-smooth muscle actin and type Ι collagen in the liver. In vitro experiments also revealed that Schizandrin C attenuated hepatic stellate cell activation in both LX-2 and HSC-T6 cells. Furthermore, lipidomics and quantitative real-time PCR analysis revealed that Schizandrin C regulated the lipid profile and related metabolic enzymes in the liver. In addition, the mRNA levels of inflammation factors were downregulated by Schizandrin C treatment, accompanied by lower protein levels of IκB-Kinase-ß, nuclear factor kappa-B p65, and phospho-nuclear factor kappa-B p65. Finally, Schizandrin C inhibited the phosphorylation of p38 MAP kinase and extracellular signal-regulated protein kinase, which were activated in the CCl4 fibrotic liver. Taken together, Schizandrin C can regulate lipid metabolism and inflammation to ameliorate liver fibrosis by nuclear factor kappa-B and p38/ERK MAPK signaling pathways. These findings supported Schizandrin C as a potential drug for liver fibrosis.

Gomisin D alleviates liver fibrosis through targeting PDGFRß in hepatic stellate cells.

Platelet-derived growth factor receptor ß (PDGFRß) plays an important role in hepatic fibrosis and is closely associated with hepatic stellate cells (HSCs) activation. Previously, by modeling PDGFRß affinity chromatography, we found that gomisin D can target PDGFRß. However, whether gomisin D has anti-fibrosis effects through targeting PDGFRß remained unclear. In this study, the effect of gomisin D on hepatic fibrosis was evaluated in vivo and vitro. HSC cell lines and primary HSC were cultured and functionally we found that gomisin D promotes HSC apoptosis, inhibits HSCs activation and proliferation. A male BALB/c mouse liver fibrosis model was established to comfirm gomisin D (especially in 50 mg/kg) could improve liver fibrosis by inhibiting HSCs activation. In addition, gomisin D had a good binding ability with PDGFRß (KD = 3.3e-5 M). Mechanically, gomisin D regulated PDGF-BB/PDGFRß signaling pathway by targeting PDGFRß, further more inhibited HSC activation, subsequently inhibited inflammatory factors, ultimately improved CCl4-induced liver fibrosis. Overall, gomisin D could inhibit HSC proliferation and activation, promote HSC apoptosis, and alleviate CCl4-induced hepatic fibrosis by targeting PDGFRß and regulating PDGF-BB/PDGFRß signaling pathway. This study provides a new drug for anti-liver firbosis therapy, and elucidates the deeper mechanism of gomisin D against HSCs activation by targeting PDGFRß.

Characterization of Cuticular Wax in Tea Plant and Its Modification in Response to Low Temperature.

Cuticular wax ubiquitously covers the outer layer of plants and protects them against various abiotic and biotic stresses. Nevertheless, the characteristics of cuticular wax and its role in cold resistance in tea plants remain unclear. In our study, cuticular wax from different tissues, cultivars, and leaves during different spatio-temporal growth stages were characterized and compared in tea plants. The composition, distribution pattern, and structural profile of cuticular wax showed considerable tissue specificity, particularly in petals and seeds. During the spatial development of tea leaves, total wax content increased from the first to fifth leaf in June, while a decreasing pattern was observed in September. Additionally, the total wax content and number of wax compounds were enhanced, and the wax composition significantly varied with leaf growth from June to September. Ten cultivars showed considerable differences in total wax content and composition, such as the predominance of saturated fatty acids and primary alcohols in SYH and HJY cultivars, respectively. Correlation analysis suggested that n-hexadecanoic acid is positively related to cold resistance in tea plants. Further transcriptome analysis from cold-sensitive AJBC, cold-tolerant CYQ, and EC 12 cultivars indicated that the inducible expression of wax-related genes was associated with the cold tolerance of different cultivars in response to cold stress. Our results revealed the characterization of cuticular wax in tea plants and provided new insights into its modification in cold tolerance.

Panchromatic Organoboron Molecules with Tunable Absorption Spectra.

Panchromatic molecules, e. g. organic small molecules with wide absorption spectra, are very desirable for solar energy-related applications. Here, we report the development of a series of organoboron compounds composed of an organoboron core unit, two π-bridging units and two electron-withdrawing end-capping units. All seven molecules have the HOMO localized on the core unit and the LUMO delocalized on the whole conjugated backbone. They exhibit wide absorption spectra consisting of two strong absorption bands with the full width at half maximum of ca. 280 nm. These panchromatic compounds can be used as electron acceptors in organic solar cells. We elucidate the relationship between the chemical structures and opto-electronic properties of these organoboron panchromatic compounds. Increasing the electron-withdrawing capability of the core units results in a downshifted HOMO level as well as blueshifted long-wavelength absorption band with increased extinction coefficient. Extending the π-bridging units causes an increased HOMO level and blueshifted long-wavelength absorption band with increased extinction coefficients. Weakening the electron-withdrawing capability of the end-capping units leads to an upshifted LUMO level and blueshifted long-wavelength absorption peak with decreased extinction coefficient. This work provides insight into the absorption spectrum manipulation of panchromatic molecules and would pave the way for the development of solar energy-related applications.

An organoboron compound with a wide absorption spectrum for solar cell applications.

Organoboron compounds offer new approaches to tune the electronic structures of π-conjugated molecules. In this work, an electron acceptor (M-BNBP4P-1) is developed by endcapping an organoboron core unit with two strong electron-withdrawing groups. M-BNBP4P-1 exhibits a unique wide absorption spectrum with two strong absorption bands in the long wavelength region (λmax = 771 nm) and the short wavelength region (λmax = 502 nm), which indicate superior sunlight harvesting capability. This is due to its special electronic structure, i.e. a delocalized LUMO and a localized HOMO. Prototype solution-processed organic solar cells based on M-BNBP4P-1 show a power conversion efficiency of 7.06% and a wide photoresponse from 350 nm to 880 nm.