Bin Guo

To determine the mechanism of electro-acupuncture (EA) effect by the wingless-related integration site (Wnt)/β-catenin pathway in the guinea pig myopia model. Following myopia induction and EA, guinea pigs were treated with biometry to evaluate refraction and axial length. Hematoxylin and eosin (HE) staining was used to observe that the retina, choroid, and sclera had abnormal morphology. At 4, 6, and 8 weeks, quantitative polymerase chain reaction (qPCR) was used to identify the expression of matrix metallopeptidase-2 (MMP-2)/MMP-3/tissue inhibitor of metalloprotease-2 (TIMP-2)/TIMP-3/Wnt family member 2B (WNT2B)/WNT3A/ WNT7B/beta-catenin 1 (CTNNB1), and dickkopf wnt signaling pathway inhibitor 1 (DKK-1) mRNAs in the retina, choroid, and sclera. Western blot was used to detect the protein expression of WNT7B/2B/3A, CTNNB1 and DKK-1 in retina, choroid and sclera at 4 weeks. Enzyme-linked immunosorbent assay was used to detect the protein expression of MMP-2/TIMP-2 and MMP-3/TIMP-3 in serum at 4 weeks. Moreover, a DKK-1 inhibitor was injected into the vitreous cavity, and the expression of the above molecules was detected. EA could reduce the optic axial length and diopter and ameliorate ocular pathology, inhibited the expression of MMP-2/MMP-3 and WNT2B/WNT3A/ WNT7B/CTNNB1, while increased the expression levels of TIMP-2/TIMP-3 and DKK-1. However, the expression levels of WNT2B/WNT3A/WNT7B/CTNNB1 and MMP-2/MMP-3 were significantly increased, and the TIMP-2/TIMP-3 and DKK-1 expression levels were decreased after injected DKK-1 inhibitor. The mechanism of EA's effects on myopia may involve the downregulation of the Wnt/β-catenin pathway and correct MMP-2/MMP-3/TIMP-2/TIMP-3 balance.

Objective: Melanoma, with its high degree of malignancy, stands as one of the most dangerous skin cancers and remains the primary cause of death from skin cancer. With studies demonstrating the potential of traditional Chinese medicine to intervene and treat melanoma, we turned our attention to celastrol. Celastrol is a triterpene compound extracted from the traditional Chinese medicine derived from Tripterygium wilfordii. Previous studies have shown that celastrol exerts inhibitory effects on various malignant tumors, including melanoma. Hence, our goal was to clarify the impact of celastrol on cell viability, apoptosis, and cell cycle progression by elucidating its effects on the PI3K/AKT/mTOR pathway. Methods: CCK-8 and wound healing assays were used to determine the effect of celastrol on the viability and migration of B16-F10 cells. Changes in cell apoptosis, cell cycle, reactive oxygen species (ROS), and mitochondrial membrane potential were detected by flow cytometry. PI3K/AKT/mTOR pathway proteins and HIF-α mRNA expression in B16-F10 cells were detected by western blotting and qPCR. Moreover, the addition of a PI3K activator demonstrated that celastrol could inhibit the function of B16-F10 cells via the PI3K/AKT/mTOR pathway. Results: Celastrol inhibited the viability and migration of B16-F10 cells. Through the inhibition of the PI3K/AKT/mTOR pathway down-regulates the expression of HIF-α mRNA, thereby causing an increase of ROS in cells and a decrease in the mitochondrial membrane potential to promote cell apoptosis and cell cycle arrest. The inhibitory effect of celastrol on B16-F10 cells was further demonstrated by co-culturing with a PI3K activator. Conclusion: Celastrol inhibits the function of B16-F10 cells by inhibiting the PI3K/AKT/mTOR cellular pathway and regulating the expression of downstream HIF-α mRNA.