The autoimmune disease Sjögren's syndrome (SS) exhibits glandular dysfunction, a direct consequence of the overwhelming lymphocyte infiltration of exocrine glands. Excessive B and T cell activation within the exocrine glands is causally linked to the chronic inflammatory process that defines the pathogenesis of this disease. Aside from dry mouth and eyes, SS can inflict harm upon other bodily organs and systems, significantly diminishing the patient's quality of life. The clinical efficacy of Traditional Chinese Medicine (TCM) in treating SS is apparent, relieving symptoms and regulating the immune system without producing adverse reactions, demonstrating its considerable safety. The past decade's preclinical and clinical trials investigating traditional Chinese medicine's application in treating SS are summarized in this paper. TCM's approach to Sjögren's Syndrome (SS) focuses on mitigating symptoms like dry mouth, dry eyes, dry skin, and joint pain. This is achieved by regulating the over-activation of B and T cells, suppressing the autoimmune response, restoring equilibrium between pro-inflammatory and anti-inflammatory cytokines, and lessening the tissue damage caused by immune complexes targeting exocrine glands and joints, ultimately leading to improved patient outcomes and quality of life.
Utilizing proteomic methods, this study explores the efficacy and potential mechanisms of Liuwei Dihuang Pills in addressing diminished ovarian reserve (DOR). The mouse model of DOR was generated by injecting cyclophosphamide (60 mg/kg) and busulfan (6 mg/kg) intraperitoneally. Following the administration of medication, the mice underwent continuous monitoring, and the efficacy of the model was assessed via disruption of the estrous cycle. After the mice were successfully modeled, they received a 28-day gavage treatment with the Liuwei Dihuang Pills suspension. The gavage treatment concluded; four female mice were selected, and caged together with 21 male mice for each female, to ascertain the pregnancy rate. The day after the last gavage, blood and ovary samples were collected from the mice that remained. Subsequently, hematoxylin-eosin (HE) staining and transmission electron microscopy (TEM) were performed to identify and characterize the morphological and ultrastructural changes in the ovaries. Hormone and oxidation indicator serum levels were quantified using enzyme-linked immunosorbent assay. Ovarian protein expression patterns before and after the modeling procedure, and also before and after Liuwei Dihuang Pills intervention, were contrasted using quantitative proteomics techniques. A study observed that Liuwei Dihuang Pills influenced DOR mice, impacting their estrous cycle, elevating serum hormones and antioxidants, encouraging follicle development, maintaining the morphology of ovarian granulosa cell mitochondria, and increasing both the size of litters and their survival. Furthermore, the impact of Liuwei Dihuang Pills was observed in the downregulation of 12 differentially expressed proteins associated with DOR, primarily participating in lipid metabolism, the inflammatory cascade, immune system modulation, and coenzyme synthesis. Differential protein expression was notably enriched in sphingolipid metabolism, arachidonic acid metabolism, ribosomal function, ferroptosis processes, and cGMP-PKG signaling pathways. To summarize, the appearance of DOR and the use of Liuwei Dihuang Pills for DOR treatment are associated with several biological processes, including, but not limited to, oxidative stress responses, inflammatory responses, and immune system regulation. The treatment of DOR with Liuwei Dihuang Pills hinges on the interplay of mitochondria, oxidative stress, and apoptosis. YY1 and CYP4F3 may be the primary upstream targets, causing mitochondrial dysfunction and reactive oxygen species buildup, whereas the metabolism of arachidonic acid represents the main signaling pathway in drug activity.
This research investigated the relationship between coagulating cold and blood stasis syndrome and glycolysis, along with assessing the impact of Liangfang Wenjing Decoction (LFWJD) on the expression of crucial glycolytic enzymes in the rat uterus and ovaries, affected by coagulating cold and blood stasis. Metabolism agonist Employing an ice-water bath, the rat model of coagulating cold and blood stasis syndrome was successfully established. Rats underwent modeling, followed by quantitative symptom scoring. This scoring then dictated the random allocation of rats into a model group and three dosage groups of LFWJD (47, 94, and 188 g/kg/day), 10 rats in each. Ten extra rats were placed in the non-experimental group. Following four weeks of consistent gavage administration, the symptom assessment was repeated quantitatively. Through the application of laser speckle flowgraphy, researchers detected modifications in microcirculation within the ears and uteruses of rats across each designated group. The pathological morphology of rat uterine and ovarian tissues within each group was characterized via hematoxylin-eosin (HE) staining. The study examined the mRNA and protein expression of pyruvate dehydrogenase kinase 1 (PDK1), hexokinase 2 (HK2), and lactate dehydrogenase A (LDHA) in rat uterine and ovarian tissues via real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. The model group's rats exhibited signs of coagulating cold and blood stasis syndrome, including curling, reduced movement, thickened lingual veins, diminished microcirculatory blood perfusion in the ears and uterus, as evidenced by hematoxylin and eosin staining. This staining also revealed a thinned endometrium with disarrayed epithelial cell arrangement and a decline in ovarian follicle count. Treatment groups, when assessed against the model group, exhibited a reduction in coagulating cold and blood stasis. This was evident through a red tongue, less nail swelling, a lack of blood stasis at the tail, and an increase in blood perfusion within the microcirculation of the ears and uterus (P<0.005 or P<0.001). The LFWJD medium and high-dose groups displayed the most pronounced positive effects on cold and blood stasis coagulation, marked by organized columnar epithelial cells lining the uterus, and a greater number of ovarian follicles, particularly mature ones, than in the control model group. Significant upregulation of PDK1, HK2, and LDHA mRNA and protein levels was observed in the model group's uterus and ovaries (P<0.005 or P<0.001), in contrast to the downregulation seen in the LFWJD medium and high-dose groups (P<0.005 or P<0.001). A significant decrease (P<0.005 or P<0.001) was observed in mRNA levels of PDK1, HK2, and LDHA, and in protein expression of HK2 and LDHA in the uterus, along with a decrease in HK2 and PDK1 protein expression in the ovaries, for the LFWJD low-dose group. LFWJD's therapeutic action on coagulating cold and blood stasis syndrome is linked to a decrease in key glycolytic enzymes, PDK1, HK2, and LDHA, and a subsequent suppression of glycolysis in both the uterus and ovaries.
This study investigated the protective effect of Shaofu Zhuyu Decoction (SFZY) against endometriosis fibrosis in mice, focusing on the phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway as a mechanistic driver. The 85 female BALB/c mice were randomly separated into a control group, a model group, high-, medium-, and low-dose SFZY groups (SFZY-H, SFZY-M, and SFZY-L), and a gestrinone suspension group (YT). Endometriosis was modeled by injecting uterine fragments into the peritoneal cavity. Fourteen days post-modeling, mice in distinct cohorts received corresponding treatments via gavage, while the control and model groups received equal volumes of distilled water by gavage. Medicine analysis The 14-day treatment concluded. Between-group variations were explored in relation to body weight, the latency of paw withdrawal caused by heat application, and the overall weight of extracted ectopic lesions. Hematoxylin-eosin (HE) and Masson staining revealed the pathological alterations in the ectopic tissue. Measurements of mRNA levels for -smooth muscle actin (-SMA) and collagen type (-collagen-) in ectopic tissue were carried out by applying real-time PCR. Protein levels of PTEN, Akt, mTOR, phosphorylated Akt, and phosphorylated mTOR in the ectopic tissue were ascertained using Western blot. Compared to the untreated group, the modeling procedure exhibited a pattern of initial weight decline followed by an increase in mouse body weight, an augmentation in the total weight of ectopic lesions, and a decrease in paw withdrawal latency. When evaluating against the model group, SFZY and YT showed an increase in body weight, a prolongation of paw withdrawal latency, and a decrement in ectopic focus weight. Furthermore, SFZY-H and YT drug administration, specifically (P<0.001), mitigated the pathological effect and reduced the extent of collagen deposition. Vancomycin intermediate-resistance Following the modeling procedure, mRNA levels for -SMA and collagen- were elevated in the ectopic focus, unlike the untreated control. This increase was attenuated by drug intervention, most evidently within the SFZY-H and YT groups (P<0.005, P<0.001). The modeling process, relative to the blank control, caused a decrease in PTEN protein levels and an increase in the levels of Akt, mTOR, p-Akt, and p-mTOR proteins, as indicated by a statistically significant difference (P<0.001, P<0.0001). The implementation of drug treatments, particularly SFZY-H and YT, resulted in the restoration of these alterations (P<0.001). Focal fibrosis in a mouse model of endometriosis may be substantially reduced by SFZY's regulation of the PTEN/Akt/mTOR signaling pathway.
Within the context of the JAK2/STAT3 signaling pathway, this study assessed the medicated serum of Sparganii Rhizoma (SR) and Curcumae Rhizoma (CR) for its effects on the proliferation, apoptosis, migration, and inflammatory cytokine secretion of ectopic endometrial stromal cells (ESCs).