Search

Objective To study the effect of MIF in colon cancer exosomes on TGF-β1 expression in liver Kupffer cells and the intervention effect of Jianpi Xiaoai Fang (Spleen-invigorating Cancer-eliminating Formula, JPXAF) at cellular level. Methods Liver Kupffer cells were treated with exosomes of colon cancer cells; and TGF-β1 mRNA expression in liver Kupffer cells was detected by using RT-PCR. After the MIF gene expression of CT26 cells was knocked down with siRNA interference technique, the exosomes were used in the treatment of Kupffer cells; and the TGF-β1 expression level of Kupffer cells was evaluated with RT-PCR and ELISA. The expressions of MIF in CT26 cells and their exosomes were measured with RT-PCR and WR after intervention with serum containing low-, mid- and high-dose JPXAF; and TGF-β1 expression in Kupffer cells was measured by using RT-PCR and ELISA after CT26 cell exosomes were treated with serum containing JPXAF. Results TGF-β1 mRNA expression in mouse Kupffer cells was increased after CT26 exosome intervention (P < 0.05%. After knockdown of MIF gene expression in CT26 cells, the up-regulation of exosomes on TGF-β1 in Kupffer cells was weakened (P < 0.05%. 20% of the serum containing JPXAF decreased the expressions of MIF in CT26 cells and their exosomes (P < 0.05%, and reduced the up-regulation of CT26 exosomes on TGF-β1 expressions in Kupffer cells (P < 0.05%. Conclusion Exosomes of colon cancer cells could up-regulate TGF-β1 expression in liver Kupffer cells by MIF. The serum containing JPXAF could reduce the expression of TGF-β1 in liver Kupffer cells by inhibiting the expression of MIF in exosomes of colon cancer cells. [ABSTRACT FROM AUTHOR]

Major depressive disorder is a genetic susceptible disease, and a psychiatric syndrome with a high rate of incidence and recurrence. Because of its complexity concerning etiology and pathogenesis, the cure rate of first-line antidepressants is low. In recent years, accumulative evidences revealed that oxytocin act as a physiological or pathological participant in a variety of complex neuropsychological activities, including major depressive disorder. Six electronic databases (Web of Science, PubMed, Scopus, Google Scholar, CNKI, and Wanfang) were employed for researching relevant publications. At last, 226 articles were extracted. The current review addresses the correlation of the oxytocin system and major depressive disorder. Besides, we summarize the mechanisms by which the oxytocin system exerts potential antidepressant effects, including regulating neuronal activity, influencing neuroplasticity and regeneration, altering neurotransmitter release, down regulating hypothalamic–pituitary–adrenal axis, anti-inflammatory, antioxidation, and genetic effects. Increasing evidence shows that oxytocin and its receptor gene may play a potential role in major depressive disorder. Future research should focus on the predictive ability of the oxytocin system as a biomarker, as well as its role in targeted prevention and early intervention of major depressive disorder. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is catastrophic and can culminate in disability and death. The routine therapy employed in early stages of SCI currently entails surgical procedures combined with high doses of methylprednisolone (MP). MP is highly controversial for the lack of consensus on its true therapeutic effects. Resveratrol (RES) has recently been recognized as a potential and novel therapeutic drug in SCI. Herein, we investigated the effect of RES in a SCI rat‐model and found significant improvement in Basso–Beattie–Bresnahan scores. Results obtained from histological, immunohistochemistry, and ultra‐structural examinations evidenced the tremendous treatment effect of RES. On the basis of our experimental results, we hypothesize that RES could serve as an effective SCI therapeutic with prolong treatment time following injury. Resveratrol (RES) is a Traditional Chinese Medicine. It did improve spinal cord injury (SCI) by inhibiting apoptosis, whiles also instigating axonal regeneration at lesion sites. RES has the potentiality of serving as future SCI therapeutic; however, further investigations regarding its mechanistic action are warranted. [ABSTRACT FROM AUTHOR]

Objective: The objective of this study is to assess the antitumor effects of hederagenin (HDG) in liver cancer (LC) cells and explore the related mechanisms., Materials and Methods: HepG2 cells were treated with HDG and cisplatin, respectively. The CCK8 assay was used to detect cell activity, DAPI staining was used to detect the proportion of living cells, TUNEL assay to detect the proportion of apoptotic cells, flow cytometry to detect the membrane potential, fluoroscopic electron microscopy to detect microstructural changes to the mitochondrial, and western blot analysis and high-content screening to detect apoptosisrelated proteins., Results: Treatment with HDG inhibited the growth of HepG2 cells, decreased the proportion of viable cells, increased the proportion of apoptotic cells, and significantly increased the proportion of cells in the G1 phase. Fluorescence staining showed that HDG damaged the mitochondria of HepG2 cells and significantly decreased the number of mitochondria. Flow cytometry showed that HDG decreased the mitochondrial membrane potential of HepG2 cells. Observations by electron microscopy showed that HDG caused swelling and vacuole formation of the mitochondria of HepG2 cells. HDG significantly reduced the average fluorescence intensity of Bcl-2 in HepG2 cells and significantly increased that of the pro-apoptosis proteins Bax, Cytochrome-c, and Caspase-3., Conclusion: HDG induced apoptosis of HepG2 cells via the mitochondrial pathway., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background/aim: Cisplatin resistance often leads to treatment futility and elevated mortality rates in patients with lung cancer. One promising strategy to address this challenge involves the integration of traditional Chinese medicine (TCM) with chemotherapeutic drugs. Currently, the potential synergistic effect and underlying mechanism of polyphyllin II (PPII) and cisplatin combination in combating cisplatin (DDP) resistance in lung cancer remain unexplored., Materials and Methods: In this study, we established a cisplatin resistance model using A549 cells and explored the underlying mechanisms of PPII in combination with cisplatin in A549/DDP resistant cells. Specifically, we assessed the impact of PPII combined with cisplatin on A549/DDP cell proliferation, viability, and the expression of apoptosis-related proteins. To gain deeper insights into the underlying mechanism, we examined the effects of PPII and cisplatin on mitochondrial function in A549/DDP cells., Results: This combination induced cell cycle arrest at both the S phase and G 2 /M phase in A549/DDP cells, thereby promoting apoptosis. Western blotting confirmed that DDP acted synergistically with PPII to enhance the expression of apoptotic proteins, diminish the expression of anti-apoptotic proteins, and promote the expression of anti-proliferation proteins in the mitochondrial pathway of A549/DDP cells., Conclusion: The combination of PPII and cisplatin effectively modulated the mitochondrial function, thereby reversing drug resistance in A549/DDP cells. This innovative combination therapy shows significant promise as a novel strategy for overcoming cisplatin resistance in lung cancer., (Copyright © 2024, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)