Gastric cancer (GC) is the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. Currently, surgery is the treatment of choice for GC. However, the associated expenses and post-surgical pain impose a huge burden on these patients. Furthermore, disease recurrence is also very common in GC patients, thus necessitating the discovery and development of other potential treatment options. A growing body of knowledge about ferroptosis in different cancer types provides a new perspective in cancer therapeutics. Ferroptosis is an iron-dependent form of cell death. It is characterized by intracellular lipid peroxide accumulation and redox imbalance. In this review, we summarized the current findings of ferroptosis regulation in GC. We also tackled on the action of different potential drugs and genes in inducing ferroptosis for treating GC and solving drug resistance. Furthermore, we also explored the relationship between ferroptosis and the tumor microenvironment in GC. Finally, we discussed areas for future studies on the role of ferroptosis in GC to accelerate the clinical utility of ferroptosis induction as a treatment strategy for GC.

Background: Heart failure (HF) is one of the diseases that seriously threaten human health today and its mechanisms are very complex. Our study aims to confirm the optimal dose ISO-induced chronic heart failure mice model for better study of HF-related mechanisms and treatments in the future. Methods: C57BL/6 mice were used to establish mice model of chronic heart failure. We injected isoproterenol subcutaneously in a dose gradient of 250 mg/kg, 200 mg/kg, 150 mg/kg, 100 mg/kg and 50 mg/kg. Echocardiography and ELISA were performed to figure out the occurrence of HF. We also supplemented the echocardiographic changes in mice over 30 days. Results: Except group S and group E, echocardiographic abnormalities were found in other groups, suggesting a decrease in cardiac function. Except group S, myofibrolysis were found in the hearts of mice in other groups. Brain natriuretic peptide was significantly increased in groups B and D, and C-reactive protein was significantly increased in each group. Conclusion: Our research finally found that the HFrEF mice model created by injection at a dose of 100 mg/kg for 7 days was the most suitable and a relatively stable chronic heart failure model could be obtained by placing it for 21 days.

Cancer is the second most common cause of mortality in the world. One of the unresolved difficult pathological mechanism issues in malignant tumors is the imbalance of substance and energy metabolism of tumor cells. Cells maintain life through energy metabolism, and normal cells provide energy through mitochondrial oxidative phosphorylation to generate ATP, while tumor cells demonstrate different energy metabolism. Neuroendocrine control is crucial for tumor cells’ consumption of nutrients and energy. As a result, better combinatorial therapeutic approaches will be made possible by knowing the neuroendocrine regulating mechanism of how the neuroendocrine system can fuel cellular metabolism. Here, the basics of metabolic remodeling in tumor cells for nutrients and metabolites are presented, showing how the neuroendocrine system regulates substance and energy metabolic pathways to satisfy tumor cell proliferation and survival requirements. In this context, targeting neuroendocrine regulatory pathways in tumor cell metabolism can beneficially enhance or temper tumor cell metabolism and serve as promising alternatives to available treatments.

Objective: This study aims to investigate the activation of the PPARγ/NF-κB pathway and its influence on macrophage M2 polarization induced by acupuncture at the Neiguan acupoint. Additionally, it seeks to explore the potential mechanisms by which electroacupuncture treatment may facilitate the reduction of inflammation in rats subjected to myocardial ischemia-reperfusion injury (MIRI).Methods: SD rats were randomly assigned to four groups: sham operation, model, electroacupuncture, and inhibitor, with 12 rats in each group. The left anterior descending branch of the coronary artery was ligated to establish the MIRI rat model. Electroacupuncture intervention at the bilateral Neiguan acupoints commenced 24 h post-chest closure, lasting for 30 min once daily over three consecutive days. Myocardial infarction was assessed through electrocardiography, while cardiac function was evaluated via echocardiography 24 h after modeling. The morphology and structure of myocardial tissues were examined using HE staining. Myocardial tissue levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) were measured by ELISA in each group of rats. The expression of the M1 macrophage marker inducible nitric oxide synthase (iNOS) and the M2 macrophage marker arginase-1 (Arg-1) in myocardial tissues was analyzed using immunohistochemistry (IHC). Detection of macrophage polarization status in myocardial tissue by flow cytometry. Additionally, peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear transcription factor-κB (NF-κB) expression in myocardial tissues was assessed using Western blotting (WB).Results: Compared with the sham-operated group, rats in the model group exhibited a significant decrease in ejection fraction (EF) (P < 0.01), along with notable myocardial fiber damage characterized by inflammatory cell infiltration. Additionally, there was an elevated expression of IL-6, TGF-β, iNOS, CD-86 and phosphorylated p65 (p-p65) in myocardial tissue (P < 0.01, P < 0.01, P < 0.05, P < 0.05 and P < 0.01, respectively). In contrast, rats in the electroacupuncture group demonstrated an increase in EF (P < 0.01) compared to the model group. Myocardial fiber damage was significantly ameliorated, inflammatory cell infiltration was reduced. Furthermore, the expression of IL-10, TGF-β, Arg-1, CD-163 and PPARγ in cardiac muscle tissue was increased (P < 0.01, P < 0.01, P < 0.05, P < 0.05 and P < 0.01, respectively). Conversely, when compared to the electroacupuncture group, the EF of rats in the inhibitor group was significantly reduced (P < 0.05), with pronounced myocardial fiber damage and accompanying inflammatory cell infiltration. Additionally, IL-6, TGF-β, iNOS CD-86 and p-p65 expression in myocardial tissue was increased (P < 0.01, P < 0.01, P < 0.05, P < 0.05 and P < 0.01, respectively).Conclusion: Electroacupuncture may ameliorate myocardial MIRI by activating the PPARγ/NF-κB pathway, promoting polarization of macrophages towards the M2 type, and reducing inflammatory damage in myocardial tissues.

Objective: Moxibustion has been shown to protect against myocardial ischemia-reperfusion injury (MIRI) by regulating mitochondrial function. Whether it preserves the structural integrity essential for this function remains unknown. Based on the critical role of cardiolipin (CL) in mitochondrial membranes, this study aimed to investigate whether CL serves as a novel target of moxibustion-mediated cardioprotection. Methods and results: A rat model of MIRI was established by ligating the left anterior descending (LAD) coronary artery for 30 min followed by 7 days of reperfusion. Moxibustion was applied to Neiguan acupoint (PC6) every other day during reperfusion. Moxibustion exerted significant cardioprotective effects by reducing interstitial fibrosis, alleviating cardiac hypertrophy, and improving cardiac function. Mechanistically, moxibustion attenuated oxidative stress-mediated mitochondrial injury, as shown by decreased ROS, 4-hydroxynonenal (4-HNE), total oxidative status (TOS), and oxidative stress index (OSI) levels, increased total antioxidant capacity (TAC), and preserved mitochondrial cristae structure. Moreover, moxibustion restored total CL levels, concomitant with downregulation of Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1) and reduction of cytosolic cytochrome c (Cyt c). Moxibustion also upregulated AMP-activated protein kinase (AMPK) phosphorylation, an effect reversed by Compound C which also largely abolished the cardioprotective effects, suggesting AMPK involvement. Conclusion: This study provides evidence for the involvement of the AMPK-oxidative stress-CL axis in moxibustion-mediated cardioprotection, highlighting the potential of moxibustion as a non-pharmacological intervention for ischemic heart disease.