Three rearranged labdane-type diterpenoids, hypophyllins A-C (1-3), and a caged labdane diterpenoid possessing a 8,9-dioxatricyclic[4.2.1.1]decane moiety, hypophyllin D (4), as well as two new biogenetically related diterpernoids, hypophyllins E (5) and F (6), were isolated from the aerial parts of Hypoestes phyllostachya "Rosea". The absolute configurations of 1-4 were determined by X-ray diffraction analysis. The plausible biogenetic pathway for 1-4 was also proposed. Compounds 4 and 5 showed potent vasorelaxant activity on endothelium-intact thoracic aorta rings precontracted with KCl.

Through metal-free protocol, hypercrosslinked porous polyporphyrin with permanent porosity was obatined via the Friedel–Crafts alkylation of tetracarbazolylporphyrin using formaldehyde dimethyl acetal as an external cross-linker. Its chemical structure and porosity was well characterized and confirmed. The BET specific surface area value of HCP-TCPP is 1050 m2 g−1 and related dominant pore size is centered at 0.63 nm. The adsorption amount of methanol by HCP-TCPP is high up to 800 mg g−1 (about 25.0 mmol g−1) at its saturated vapor pressure, which is higher than that of toluene (600 mg g−1, 6.5 mmol g−1). Further study indicates that polymer HCP-TCPP, possessing the high BET specific surface area and total pore volume, exhibits good hydrogen uptake of 3.44 wt % (77 K) and high carbon dioxide uptake of 41.1 wt % (298 K) at 18.0 bar. Besides, the obtained porous polymer can also be used as an effective heterogeneous catalyst for the Knoevenagel condensation between various aldehydes and malononitrile.

Non-alcoholic steatohepatitis (NASH) is a common chronic liver disease worldwide, with no effective therapies available. Discovering lead compounds from herb medicine might be a valuable strategy for the treatment of NASH. Here, we discovered Alisol B, a natural compound isolated from Alisma orientalis (Sam.), that attenuated hepatic steatosis, inflammation, and fibrosis in high-fat diet plus carbon tetrachloride (DIO+CCl4)-induced and choline-deficient and amino acid-defined (CDA)-diet-induced NASH mice. RNA-seq showed Alisol B significantly suppressed CD36 expression and regulated retinol metabolism in NASH mice. In mouse primary hepatocytes, Alisol B decreased palmitate-induced lipid accumulation and lipotoxicity, which were dependent on CD36 suppression. Further study revealed that Alisol B enhanced the gene expression of RARα with no direct RARα agonistic activity. The upregulation of RARα by Alisol B reduced HNF4α and PPARγ expression and further decreased CD36 expression. This effect was fully abrogated after RARα knockdown, suggesting Alisol B suppressed CD36 via regulating RARα-HNF4α-PPARγ cascade. Moreover, the hepatic gene expression of RARα was obviously decreased in murine NASH models, whereas Alisol B significantly increased RARα expression and decreased CD36 expression, along with the downregulation of HNF4α and PPARγ. Therefore, this study showed the unrecognized therapeutic effects of Alisol B against NASH with a novel mechanism by regulating RARα-PPARγ-CD36 cascade and highlighted Alisol B as a promising lead compound for the treatment of NASH.