Efficacy of preoperative Shugan Sanjie decoction combined with mammotome-assisted minimally invasive surgery in the treatment of idiopathic granulomatous mastitis: A retrospective cohort study.

The management of idiopathic granulomatous mastitis (IGM) poses a significant challenge because of its ambiguous etiology. This study aimed to investigate the efficacy of traditional Chinese medicine (TCM) combined with mammotome-assisted minimally invasive surgery (MAMIS) for the treatment of IGM. This retrospective cohort study included patients with IGM who underwent treatment at our hospital between January 2017 and June 2022. Patients treated with Shugan Sanjie decoction alone and preoperative Shugan Sanjie decoction combined with MAMIS were included in Groups A and B, respectively. We focused on the demographics, clinical characteristics, and outcomes of the patients in the 2 groups. A total of 124 female patients with an average age of 33.9 ± 3.6 years were included in the study. The demographic and clinical characteristics of patients in Groups A (n = 55) and B (n = 69) were similar (P > .05). However, there were significant differences between the 2 groups in terms of treatment duration, 1-year complete remission (CR), and recurrence. Group B showed shorter treatment time (11.7 ± 5.1 vs 15.3 ± 6.4 months, P = .001), higher 1-year CR (72.5% vs 45.5%, P = .002), and lower recurrence (7.2% vs 21.8%, P = .019) in comparison to Group A. Shugan Sanjie decoction promoted the shrinkage of breast lesions in patients with IGM. Combined with MAMIS, this treatment regimen shortened the treatment duration, accelerated the recovery process, and reduced the recurrence rate.

Prim-O-glucosycimifugin attenuates liver injury in septic mice by inhibiting NLRP3 inflammasome/caspase-1 signaling cascades in macrophages.

BACKGROUND: Liver dysfunction and liver failure are serious complications of sepsis, directly leading to septic progression and death. Now, there is no specific therapeutics available for sepsis-related liver dysfunction. Prim-O-glucosylcimifugin (POG), a chromone richest in the roots of Saposhnikovia divaricata (Turcz.) Schischk, is usually used to treat headache, rheumatoid arthritis and tetanus. While, the underlying mechanisms of POG against sepsis-induced liver damage and dysfunction are still not clear. PURPOSE: To study the anti-sepsis effect of POG, and its pharmacological mechanism to protect liver injury by weakening the function of macrophages in septic livers through inhibiting NOD-like receptor protein 3 (NLRP3) inflammasome pathway. METHOD: In vivo experiments, septic mouse model was induced by cecal ligation and puncture (CLP), and then the mortality was detected, liver inflammatory damages and plasma biomarkers of liver injury were evaluated by histopathological staining and biochemical assays, respectively. In vitro experiments, mouse primary peritoneal macrophages were treated with lipopolysaccharide (LPS) and ATP, and then the activated-inflammasomes, macrophage migration and polarization were detected by ASC immunofluorescence staining, transwell and flow cytometry assays, respectively. NLRP3 inflammasome components NLRP3, caspase-1, IL-1ß and IL-18 protein expressions were detected using western blot assays, and the contents of IL-1ß and IL-18 were measured by ELISA assays. RESULTS: POG treatment significantly decreased the mortality, liver inflammatory damages, hepatocyte apoptosis and plasma biomarkers of liver injury in CLP-challenged male WT mice, which were comparable to those in ibuprofen (a putative anti-inflammatory drug)-supplemented septic male WT mice and septic NLRP3 deficient-male mice. POG supplementation significantly suppressed NLRP3 inflammasome activation in septic liver tissues and cultured macrophages, by significantly reducing NLRP3, cleaved-caspase-1, IL-1ß and IL-18 levels, the activated-inflammasome ASC specks, and macrophage infiltration and migration, as well as M1-like polarization, but significantly increasing M2-like polarization. These findings were similar to the pharmacological effects of ibuprofen, NLRP3 deficiency, and a special NLRP3 inhibitor, MCC950. CONCLUSION: POG protected against sepsis by inhibiting NLRP3 inflammasome-mediated macrophage activation in septic liver and attenuating liver inflammatory injury, indicating that it may be a potential anti-sepsis drug candidate.

Mogrol suppresses lung cancer cell growth by activating AMPK-dependent autophagic death and inducing p53-dependent cell cycle arrest and apoptosis.

Lung carcinoma is the leading cause of cancer-related death worldwide. Chemotherapy remains the cornerstone of lung cancer treatment. Unfortunately, most types of cancer will develop resistance to chemotherapies over the time. One of the efforts to prevent the chemotherapy resistance is to find alternative chemotherapy drugs. Mogrol has been found to have antitumor activity. However, little is known about the pharmacological mechanisms underlying the suppression of mogrol on lung cancers. In this study, we observed that mogrol exposure significantly reduced the tumor volume and weight in tumor-bearing nude mice without obvious effect on body weight and cardiac function. Mogrol also significantly inhibited the proliferation and migration of lung cancer cells, including non-small-cell lung carcinoma cells, A549, H1299, H1975 and SK-MES-1 cells, with no obvious effect on control human bronchial epithelial cells (HBE). Further studies revealed that mogrol stirred excessive autophagy and autophagic flux, and finally, autophagic cell death, in lung cancer cells, which could be attenuated by autophagy inhibitors, 3-MA and chloroquine. Furthermore, mogrol significantly activated AMPK to induce autophagy and autophagic cell death, which could be abrogated by Compound C, an AMPK inhibitor. In addition, mogrol induced a significant increase in p53 activity in lung cancer cells, accompanied with cell cycle arrest and apoptosis, which could be weakened by p53 silence. Our results indicated that mogrol effectively suppressed lung cancer cells in vivo and in vitro by inducing the excessive autophagy and autophagic cell death via activating AMPK signaling pathway, as well as cell cycle arrest and apoptosis via activating p53 pathway.

The molecular landscape of histone lysine methyltransferases and demethylases in non-small cell lung cancer.

Background: Lung cancer is one of the most common malignant tumors. Histone methylation was reported to regulate the expression of a variety of genes in cancer. However, comprehensive understanding of the expression profiles of histone methyltransferases and demethylases in lung cancer is still lacking. Methods: We analyzed the expression profile of methyltransferases and demethylases in non-small cell lung cancer (NSCLC) using TCGA and cBioportal databases. The mutation, expression level, association with survival and clinical parameters of histone methyltransferases and demethylases were determined. Results: We found overall upregulation of histone regulators in NSCLC. Mutation and copy number alteration of histone methylation related genes both exist in NSCLC. The expression of certain histone methylation related genes were significantly associated with overall survival and clinical attributes. Conclusions: Our result suggests that alteration of histone methylation is strongly involved in NSCLC. Some histone methylation related genes might serve as potential prognosis predictor or therapeutic target for NSCLC. The significance of some histone methylation related genes was contrary to the literature and awaits further validation.

Stem cells responsible for deer antler regeneration are unable to recapitulate the process of first antler development-revealed through intradermal and subcutaneous tissue transplantation.

Antlers offer a unique model for the study of whether regeneration recapitulates development in a mammalian organ. Research, to date, supports the full recapitulation in antler, but a recent report that subcutaneously transplanted (ST) pedicle periosteum (PP) failed to induce that ectopic antler formation could argue against recapitulation, as antlerogenic periosteum (AP) can readily do so. However, it was not clear in that study whether the result was caused by inability of the PP to interact with the skin or owing to failure to create the required close contact to it. This study was designed to clarify this uncertainty by adopting intradermal transplantation (IT) to achieve the required close contact without the need for significant mass expansion. The results showed that IT of 1/8 of the original AP mass or more was sufficient for antler induction, whereas ST of 1/4-AP or less could not do so within 2 years. The minimum amount of AP required for antler induction using the IT approach was somewhere between 1/8 and 1/12-AP (<30 mg). The results further demonstrated that IT of 62-84 mg PP failed to induce ectopic antler formation, even if the PP had fused with the surrounding skin. Because this mass of PP was 2-3 times the minimum amount of AP required for antler induction, we conclude that PP does not recapitulate AP in induction of ectopic antler development. It is likely that PP has been restricted for antler regeneration and lost the potential to initiate antler development.