Objective To observe the effects of camellia oil on the development of allergic contact dermatitis in mice. Methods Mice models of allergic contact dermatitis were established with dinitrofluo-robene (DNFB). Then, certain concentrations of camellia oil and halcinonide were used topically on the ears of mouse models twice daily for 6 days. Skin specimens were obtained from the treated ears and subjected to histology examination and pathological analysis. RT-PCR was performed to detect the mRNA expressions of interleukin 2 (IL-2) and interferon γ (IFN-γ) in the skin tissues. Results Allergic contact dermatitis was successfully induced by DNFB in mice with a marked increase in the mRNA expression of IL-2 and IFN-7. There was a slight decrease in the ear swelling degree, inflammatory reaction intensity, number of infiltrating inflammatory cells, and pathological severity in camellia oil-treated mice and halcinonide-treated mice compared with glycerinetreated mice. Camellia oil and halcinonide also induced different degrees of reduction in the mRNA expression of IL-2 and IFN-γ in inflammatory tissues. Conclusion Camellia oil can alleviate the pathological damage and down-regulate the expression of IL-2 and IFN-7 in mice with DNFB-induced allergic contact dermatitis.

Traditional Chinese Medicine (TCM) exerts anti-tumor effects by intervening in A549 cells of human lung adenocarcinoma, mainly including activating or inhibiting downstream target proteins of Bcl-2 and Bax, or forming RIP1/RIP3/MLKL complex bodies by affecting pathways such as PI3K/Akt, thereby inducing apoptosis in A549 cells of lung adenocarcinoma; blocks the cell growth phase, thereby inhibiting the proliferation of lung adenocarcinoma A549 cells; inhibits invasion and metastasis of A549 cells by affecting the MMPs pathway, STAT3 pathway, and regulating epithelial mesenchymal transition related factors; suppresses or activates the expression of related proteins or affect related signaling pathways, thereby reversing the resistance of lung cancer A549/DDP cell lines to cisplatin and paclitaxel.

In vitro cell experiment based on serum pharmacology is a common way to study the pharmacodynamic mechanism of Chinese medicine， and screening the optimal intervention concentration of serum containing Chinese medicine is a key step in the whole experiment. Over-diluted serum containing Chinese medicine or over-high concentration leads to false negative or positive results， while the optimal concentration of medicated serum reduces the number of groups in subsequent experiments as well as the operation error. Thus it is of great significance to screen the optimal serum concentration in studying the pharmacodynamic mechanism of Chinese medicine in in vitro cell experiments. However， there has been no unified standards for the screening methods at present. After reviewing the literature in China and abroad in the past 20 years， this paper conducted an analysis from three aspects of intragastric dose of Chinese medicine， blood collection time and serum dilution degree， and then summarized the screening methods for optimal concentration of serum containing drugs， providing guidance for the study of pharmacodynamic mechanism of Chinese medicine. The screening methods mainly included "same intragastric dose， same blood collection time， and different concentrations" "different intragastric doses， same blood collection time， and same concentration" "same intragastric dose， different blood collection time， and same concentration" "different intragastric doses， different blood collection time， and different concentrations" "serum lyophilized powder" "simulation of gradient concentration of serum containing western medicine" and "pure serum intervention". Among them， the former two were the dominant ways in current related research. The above screening methods had their own advantages and disadvantages， and researchers should make a reasonable choice according to the specific requirements and actual situation of the experiments.

ERK pathway regulated the programmed death ligand-1 (PD-L1) expression which was linked to the response of programmed death-1 (PD-1)/PD-L1 blockade therapy. So it is deducible that ERK inhibitor could enhance the efficacy of PD-1 inhibitor in cancer immunotherapy. In this study, PD0325901, an oral potent ERK inhibitor, strongly enhanced the efficacy of PD-1 antibody