Abatract:Objective To observe the structure of human skin equivalent (HSE)model in vitro,and to preliminarily assess the barrier function of HSE.Methods The HSE model was established by two steps:preparation of dermal layer and preparation of full-thickness skin.Keratinocytes were inoculated on the surface of dermal layer prepared by type 1 collagen coating fibroblasts.After submerged cultured for one week,air-liquid interface cultured for three weeks to enhance the proliferation of keratinocytes,the HSE model was obtained.Then the macroscopical structure and electon microscopical structure of HSE were studied.To investigate the barrier function of HSE model,indometacin was selected as the model drug for the penetration testing in vitro.Results The structures similar to dermal layer and epidermal layer of human skin were developed in HSE model,furthermore,complete straum corneum with similar ultrastructure of human skin was developed on the surface of epidermal layer.The penetration testing showed that the barrier function of HSE was slightly lower than that of rat abdominal skin within 24 h,but the cumulative content (Q24 )of indometacin of HSE was far slower (only 28%)than rat abdominal skin from 22 to 24 h.However,the steady state flux of indometacin showed no significant difference in HSE model and rat abdominal skin(P >0.05).Conclusion The morphology and structure of HSE model were close to human skin;and in HSE model,the barrier function against indometacin was almost as the same as the rat abdominal skin.It is expected that HSE model be an alternative option of animal skin to evaluate the effect of transdermal drug delivery system.

As one of the most common solid organ malignant tumors in the world， hepatocellular carcinoma has climbed to the fourth place in incidence rate and the second place in mortality in China， which seriously threatens people’s health. Terpenoids are natural active substances widely present in nature， among which sesquiterpenoids are numerous. They exhibit a variety of pharmacological activities， such as anti-tumor， antibacterial， anti-inflammatory， antiviral and antioxidant activities. This article reviews the research progress on the anti-hepatocellular carcinoma mechanism of sesquiterpenes from 2015 to 2024. The results showed that 24 sesquiterpenoids for the treatment of hepatocellular carcinoma have been reported in the literature in the past 10 years， and these compounds have shown potential in treating hepatocellular carcinoma by inhibiting cancer cell proliferation， inducing apoptosis， preventing invasion and metastasis， regulating immunity， and enhancing anti-drug resistance. The mechanism of anti-hepatocellular carcinoma mainly involves three regulatory pathways: phosphatidylinositol 3-kinase/protein kinase B/ mammalian target of rapamycin signaling pathway， nuclear factor kappa-B signaling pathway， and mitochondrial pathway. In the future， it is necessary to continue to explore new anti-hepatocellular carcinoma drugs with high research value， conduct in-depth analysis on the mechanism of synergistic anti-hepatocellular cancer effects of multiple components， targets， pathways， and accelerate the development of finished products in order to be widely used in clinical practice.

As a member of the Sirtuins family in mammals, SIRT7 locates in nucleus and is a highly specific H3K18Ac (acetylated lysine 18 of histone H3) deacetylase. Recent studies showed that SIRT7 could participate in the ribosomal RNA transcription, cell metabolism, cell stress and DNA damage repair through various signaling pathways. In addition, SIRT7 is also closely related with aging, heart disease and fatty liver. In particular, SIRT7 plays important roles in the regulation of initiation and development of various tumors, such as liver cancer, gastric cancer, breast cancer, bladder cancer, colorectal cancer, and head/neck squamous cell carcinoma. This review describes the cellular and molecular functions of SIRT7, and systematically summarizes recent progress of SIRT7 in human disease.
Animals ; Histones ; Humans ; Lysine ; Neoplasms ; Signal Transduction ; Sirtuins ; metabolism