ABSTRACT
Diosgenin, a steroidal sapogenin, obtained from Trigonella foenum-graecum, Dioscorea, and Rhizoma polgonati, has shown high potential and interest in the treatment of various cancers such as oral squamous cell carcinoma, laryngeal cancer, esophageal cancer, liver cancer, gastric cancer, lung cancer, cervical cancer, prostate cancer, glioma, and leukemia. This article aims to provide an overview of the in vivo, in vitro, and clinical studies reporting the diosgenin's anticancer effects. Preclinical studies have shown promising effects of diosgenin on inhibiting tumor cell proliferation and growth, promoting apoptosis, inducing differentiation and autophagy, inhibiting tumor cell metastasis and invasion, blocking cell cycle, regulating immunity and improving gut microbiome. Clinical investigations have revealed clinical dosage and safety property of diosgenin. Furthermore, in order to improve the biological activity and bioavailability of diosgenin, this review focuses on the development of diosgenin nano drug carriers, combined drugs and the diosgenin derivatives. However, further designed trials are needed to unravel the diosgenin's deficiencies in clinical application.
Subject(s)
Carcinoma, Squamous Cell , Diosgenin , Mouth Neoplasms , Prostatic Neoplasms , Male , Humans , Carcinoma, Squamous Cell/drug therapy , Diosgenin/pharmacology , Diosgenin/therapeutic use , Diosgenin/metabolism , Mouth Neoplasms/drug therapy , Apoptosis , Prostatic Neoplasms/drug therapyABSTRACT
Accumulating evidence has shown that allogeneic blood transfusions can induce significant immunosuppression in recipients, and thereby increase the risk of postoperative infection and/or tumor relapse. Although it is well known that natural killer (NK) cells are responsible for the immunodepression effects of transfusion, the underlying mechanisms remain obscure. In this study, we investigated the role of NK cells in transfusion-induced immunodepression in ß-thalassemia major. The proportion of circulating NK cells and the expression of NK receptors (NKG2A, CD158a, NKP30, NKP46 and NKG2D) as well as CD107a were detected by multicolor flow cytometry. IFN-γ production by circulating NK cells was detected by intracellular cytokine staining. Our results showed that the proportion and cytotoxicity (CD107a expression) of circulating NK cells in transfusion-dependent ß-thalassemia major patients were remarkably lower than those of ß-thalassemia minor patients or healthy volunteers. Expression of NKG2A inhibitory receptor on circulating NK cells in patients with ß-thalassemia major was remarkably up-regulated, but there were no significant differences in the expression levels of NKP30, NKP46, NKG2D, CD158a and IFN-γ. These results indicate NKG2A inhibitory receptor may play a key role in transfusion-induced immunodepression of NK cells in patients with ß-thalassemia major.
Subject(s)
Killer Cells, Natural/metabolism , NK Cell Lectin-Like Receptor Subfamily C/blood , beta-Thalassemia/blood , beta-Thalassemia/immunology , Adolescent , Child , Female , Flow Cytometry , Gene Expression Regulation , Humans , Immunosuppression Therapy , Killer Cells, Natural/immunology , Male , NK Cell Lectin-Like Receptor Subfamily C/immunology , NK Cell Lectin-Like Receptor Subfamily K/blood , NK Cell Lectin-Like Receptor Subfamily K/immunology , Natural Cytotoxicity Triggering Receptor 1/blood , Natural Cytotoxicity Triggering Receptor 1/immunology , Natural Cytotoxicity Triggering Receptor 3/blood , Natural Cytotoxicity Triggering Receptor 3/immunology , Receptors, KIR2DL1/blood , Receptors, KIR2DL1/immunology , Transfusion Reaction , beta-Thalassemia/pathologyABSTRACT
OBJECTIVE: To investigate the hepatic expression of immunological markers relevant to a cytotoxic response in relation to viral genotype. METHODS: The frozen liver biopsies were obtained from 28 HF genotyped patients and made the sections stained. The morphometry was used to analyze the major histocompatibility complex class I (MHC-I), CD8, beta(2)-microglobulin (beta(2) -mG), HFE and CD68 in the stained sections. Biopsy data of response to therapy with interferon were available in 18 cases. RESULTS: CD8+ was usually clustered together and localized in portal tracts and sinusoids, and seen to interact with MHC I positive lining cells. MHC-I and beta(2) -mG were expressed mainly in endothelial and Kupffer cells. HFE was expressed in most round and dendritic CD68+ cells. Patients with virus genotype 3a had higher hepatic MHC-I and HFE expression, and a better sustained response to interferon (IFN) therapy than patients without. CONCLUSION: The MHC-I expression in the liver of patient with chronic hepatitis C virus infection seems to relate to viral-genotype. The hepatic MHC-I and HFE expression are higher in patients with virus genotype 3a than that in patients with non-3a genotype.
