Current drug delivery · 2026
Study on the Preparation of Frankincense Volatile Oil Submicro Emulsion and Its Effect on Ulcerative Colitis.
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Liu Mei, Wang Yujiao, Wang Mengmeng, Zhang Le, Niu Zihao, Wang Xuan, Wang Jie, Xia Ning, Wang Jinhui, Ge Xiaoxiao, Chen Chao, Chen Qin, Zhang Shihao, Xie Yundong, Shi Huanxian, Zhao Chongbo, Zou Junbo, Guo Dongyan, Shi Yajun, Yang Ming, She Zhennan, Zhang Xiaofei, Sun Jing
Аннотация
INTRODUCTION: Frankincense Essential Oil (FREO) has demonstrated curative potential in Ulcerative Colitis (UC) patients. However, the inherent instability of FREO results in its relatively low bioavailability. Therefore, the present study aimed to develop a novel oral O/W type FREO Submicron Emulsion Formulation (FREO-SE). This was achieved by encapsulating FREO within submicron emulsion droplets, with the further objective of elucidating the anti-UC efficacy of FREOSE.
METHODS: A single-factor experimental approach was employed to screen the formulation, dosage, and preparation process of FREO-SE. Subsequently, the Box-Behnken Design (BBD) was utilized to optimize the submicron emulsion preparation procedure. The quality of the prepared emulsion was evaluated. Finally, a comparative analysis of the anti-ulcerative colitis efficacies of FREO and FREOSE was conducted using a UC mouse model. The mechanism of action of FREO-SE was further examined through immunohistochemistry, with the ultimate goal of enhancing the stability of FREO and elucidating its therapeutic effects on ulcerative colitis.
RESULTS: The optimal formulation and manufacturing process for FREO-SE were established, and the particle size, PDI, and Zeta potential were characterized, with values of 105.09 ± 1.27 nm, 0.30 ± 0.02, and -37.43 ± 0.97 mV, respectively, confirming the successful preparation of FREO-SE. In DSS-induced UC mice, FREO-SE significantly reduced the DAI score compared with the DSS group. The weight loss of the FREO-SE-H group mice was significantly reduced (p < 0.001), and the shortening of colon length was significantly reduced (p < 0.001). Serum TNF-α and IL-6 levels were significantly reduced (p < 0.001), thereby alleviating colonic tissue lesions. The expression of p-ERK and p-P65 in colon tissue was significantly reduced (p < 0.001). In conclusion, FREO-SE inhibited the levels of p-ERK and p-P65 in MAPK and NF-κB signaling, and demonstrated a definite therapeutic effect in a mouse model of ulcerative colitis.
DISCUSSION: This study confirmed that the FREO-SE formulation notably potentiates the therapeutic efficacy of FREO against UC, with its mechanism underlying modulation of the MAPK/NF-κB inflammatory signaling pathway.
CONCLUSION: The preparation process of FREO-SE is characterized by stability, simplicity, and controllability, endowing it with excellent stability. FREO-SE exhibits a protective effect against DSSinduced UC in mice and demonstrates significant efficacy in the ulcerative colitis mouse model.
METHODS: A single-factor experimental approach was employed to screen the formulation, dosage, and preparation process of FREO-SE. Subsequently, the Box-Behnken Design (BBD) was utilized to optimize the submicron emulsion preparation procedure. The quality of the prepared emulsion was evaluated. Finally, a comparative analysis of the anti-ulcerative colitis efficacies of FREO and FREOSE was conducted using a UC mouse model. The mechanism of action of FREO-SE was further examined through immunohistochemistry, with the ultimate goal of enhancing the stability of FREO and elucidating its therapeutic effects on ulcerative colitis.
RESULTS: The optimal formulation and manufacturing process for FREO-SE were established, and the particle size, PDI, and Zeta potential were characterized, with values of 105.09 ± 1.27 nm, 0.30 ± 0.02, and -37.43 ± 0.97 mV, respectively, confirming the successful preparation of FREO-SE. In DSS-induced UC mice, FREO-SE significantly reduced the DAI score compared with the DSS group. The weight loss of the FREO-SE-H group mice was significantly reduced (p < 0.001), and the shortening of colon length was significantly reduced (p < 0.001). Serum TNF-α and IL-6 levels were significantly reduced (p < 0.001), thereby alleviating colonic tissue lesions. The expression of p-ERK and p-P65 in colon tissue was significantly reduced (p < 0.001). In conclusion, FREO-SE inhibited the levels of p-ERK and p-P65 in MAPK and NF-κB signaling, and demonstrated a definite therapeutic effect in a mouse model of ulcerative colitis.
DISCUSSION: This study confirmed that the FREO-SE formulation notably potentiates the therapeutic efficacy of FREO against UC, with its mechanism underlying modulation of the MAPK/NF-κB inflammatory signaling pathway.
CONCLUSION: The preparation process of FREO-SE is characterized by stability, simplicity, and controllability, endowing it with excellent stability. FREO-SE exhibits a protective effect against DSSinduced UC in mice and demonstrates significant efficacy in the ulcerative colitis mouse model.