Depressive disorder is a common psychiatric condition clinically characterized by impaired cognitive function， which profoundly affects patients' daily living and social functioning. Despite extensive research on the mechanism underlying the interaction between ghrelin and depressive disorder， comprehensive reviews， summary， and systematic organization of these findings remain lacking. To address this gap， this study aims to conduct a systematic evaluation of the effects and mechanisms of ghrelin on cognitive function in patients with depressive disorder， thereby providing references for targeted clinical interventions. On October 20， 2024， literature exploring the role and mechanisms of ghrelin in improving cognitive function in depressive disorder was sourced from the CNKI， PubMed and Web of Science databases， covering the period from the inception of the database till October 20， 2024. Two researchers independently conducted literature screening and data extraction. Ultimately， 9 articles were included in this review. The findings suggest that ghrelin improves cognitive function in patients with depressive disorder through multiple mechanisms， including mitigating inflammatory responses， modulating oxidative stress， and activating the cyclic adenosine monophosphate response element binding protein-brain-derived neurotrophic factor （CREB-BDNF） signaling pathway.

Objective:To investigate the effect of gap junction protein Cx43 inhibitor carbenoxolone (CBX) on cognitive function and its possible mechanism in epileptic rats.Methods:One hundred and twenty Wistar rats were randomly divided into sham-operated group, epilepsy group, epilepsy+solvent group, and epilepsy+CBX group ( n=30). The models of temporal lobe epilepsy in the later three groups were prepared by injection of kainic acid in the hippocampus. Intraperitoneal injection of CBX (20 mg/kg) or equal amount of normal saline were given to the rats in the epilepsy+CBX group and epilepsy+solvent group 30 min before modeling. Western blotting was used to detect the protein expressions of phosphorylated (p)-Cx43 and microtubule associated protein light chain 3 (LC3) in the hippocampus 6, 12, and 24 h after modeling; the protein localization of p-Cx43 and LC3 in the hippocampus and optical density of their positive cells were detected by immunohistochemistry 24 h after modeling; the learning and memory abilities of rats were tested by Morris water maze experiment 30 d after modeling. Results:Western blotting results showed that as compared with those in the sham-operated group, p-CX43 and LC3 protein expressions in the hippocampal CA3 regions of epilepsy group and epilepsy+solvent group were significantly increased at 6, 12 and 24 h after modeling ( P<0.05); as compared with the epilepsy group and epilepsy+solvent group, the epilepsy+CBX group had statistically decreased p-CX43 and LC3 protein expressions in the hippocampal CA3 regions at each time point ( P<0.05). Immunohistochemical staining showed that p-CX43 was localized at the cell membrane and cytoplasm of hippocampal astrocytes; LC3 was located at the cytoplasm of hippocampal neurons. As compared with those in the sham-operated group, the optical density values of p-CX43 and LC3 positive cells in hippocampal CA3 regions of epilepsy group and epilepsy+solvent group were increased ( P<0.05). As compared with those in the epilepsy group and the epilepsy+solvent group, the optical density values of p-CX43 and LC3 positive cells in the hippocampal CA3 regions of the epilepsy+CBX group were significantly decreased ( P<0.05). Morris water maze test results showed that as compared with that in the sham-operated group, the escape latency in the epilepsy group and epilepsy+solvent group was significantly prolonged ( P<0.05); as compared with that in the epilepsy group and epilepsy+solvent group, the latency in the epilepsy+CBX group was significantly shortened ( P<0.05). Conclusion:CBX can weaken the neuronal autophagy and reduce the damage to cognitive function by inhibiting the p-Cx43 protein expression in the astrocytes of the hippocampal CA3 regions.

Objective To investigate the molecular mechanism of miR-139-5p targeting transforming growth factor-β1 (TGF-β1) in the regulation of epithelial mesenchymal transition (EMT),thus inhibiting invasion and metastasis of hepatoma cells.Methods Bioinformatics methods were used to determine whether miR-139-5p was the best binding miRNA of TGF-β1.Correlation between the TGF-β1 expression as detected by immunohistochemistry and Western blot,and the miR-139-5p level by qRT-PCR in 56 hepatoma tissues and 20 normal tissues,respectively,was analyzed.The relationship between the miR-139-5p level as detected by qRT-PCR,and TGF-β1,E-cadherin and Vimentin by Western blot in the high and low metastatic hepatoma cell lines were investigated.In recombinant cell lines,whether miR-139-5p could bind to the 3'UTR site of TGF-β1 was evaluated,and the effect on invasive ability after modulating miR-139-5p level was also tested by the transwell method.Results A total of 20 miRNAs were found to be able to bind with TGF-β1 by bioinformatics methods and among these mRNAs,miR-139-5p was the best target miRNA with the highest specificity and strongest stability to bind TGF-β1.The positive expression rates of TGF-β1 in hepatoma tissues and adjacent normal liver tissues were 80.4％ (45/56) and 15.0％ (3/20),respectively,(P ＜0.05).There were significant differences on the expressions of TGF-β1,E-cadherin and Vimentin among the different metastatic cell lines (all P ＜ 0.05).After miR-139-5p was transfected into hepatoma cells,miR-139-5p could bind to the 3'UTR site of TGF-β1,resulting in downregulating TGF-β1 expression.When compared to the other three groups,the cell line with a high expression of miR-139-5p had a significantly lower count of invasive cells (53 ± 4/high magnification field) (P ＜ 0.05).Conclusion miRNA139-5p could specifically bind to the 3'UTR site of TGF-β1 and regulate the EMT signaling pathway,thus suppressing invasion and metastasis of hepatoma cells.