Its botany, ethnopharmacology, phytochemistry, pharmacological properties, toxicology, and quality assurance measures are investigated to reveal its effects and establish a foundation for subsequent research.
Historically, Pharbitidis semen has served as a deobstruent, diuretic, and anthelmintic in various tropical and subtropical medicinal traditions. The extraction procedure successfully isolated 170 different chemical compounds, categorized as terpenoids, phenylpropanoids, resin glycosides, fatty acids, and further chemical compounds. Studies have revealed that this substance possesses multiple effects, including laxative, renal-protective, neuroprotective, insecticidal, antitumor, anti-inflammatory, and antioxidant properties. Beyond that, a brief introduction to the subjects of processing, toxicity, and quality control is provided.
Though traditionally used for diarrhea, the bioactive and harmful components of Pharbitidis Semen continue to be a subject of research and are not yet fully understood. Improving the identification of active components in Pharbitidis Semen and the research behind them is vital, as is a deeper understanding of the molecular mechanisms of its toxicity and how to modulate the body's internal substances to enhance its safe and effective use in clinical applications. Compounding the matter, the deficient quality standard demands an immediate solution. Modern pharmacological research has broadened the deployment of Pharbitidis Semen, showcasing possibilities for maximizing its efficacy and use.
Pharbitidis Semen's age-old use in managing diarrhea has been shown to be effective, however, the particular bioactive and potentially toxic compounds within it are not definitively characterized. Further investigation into the potent constituents and natural bioactive compounds within Pharbitidis Semen, coupled with a deeper understanding of its toxicity mechanisms and the modification of endogenous substance rules, is essential to improve its clinical utility. Moreover, the deficiency in quality standards constitutes a challenge that requires immediate action. Expanding the scope of modern pharmacology, Pharbitidis Semen has seen its applications broadened, along with ideas for improved resource management.
Kidney deficiency, as posited by Traditional Chinese Medicine (TCM) theory, is the underlying cause of the chronic refractory asthma, complete with airway remodeling. While our prior experiments with Epimedii Folium and Ligustri Lucidi Fructus (ELL), impacting kidney Yin and Yang equilibrium, indicated a reduction in airway remodeling pathology in asthmatic rats, the specific method by which this effect occurs remains unknown.
This research project was undertaken to illuminate the interplay between ELL and dexamethasone (Dex) regarding the proliferation, apoptosis, and autophagy of airway smooth muscle cells (ASMCs).
Rat ASMC primary cultures, at passages 3-7, were treated with histamine (Hist), Z-DEVD-FMK (ZDF), rapamycin (Rap), or 3-methyladenine (3-MA) for either 24 or 48 hours. Subsequently, the cells were exposed to treatments comprising Dex, ELL, and ELL&Dex, for a period of either 24 or 48 hours. TI17 Cell viability was determined by the Methyl Thiazolyl Tetrazolium (MTT) assay, evaluating the effects of various inducer and drug concentrations. Immunocytochemistry (ICC) using Ki67 protein was used to quantify cell proliferation. Cell apoptosis was measured by the Annexin V-FITC/PI assay, in conjunction with Hoechst nuclear staining. Transmission electron microscopy (TEM) and immunofluorescence (IF) were employed to visualize cell ultrastructure. Finally, Western blot (WB) combined with quantitative real-time PCR (qPCR) analyzed the expression levels of autophagy and apoptosis-related genes, including protein 53 (P53), caspase-3, LC3, Beclin-1, mammalian target of rapamycin (mTOR), and p-mTOR.
Cell proliferation in ASMCs was promoted by Hist and ZDF, coupled with a significant reduction in Caspase-3 protein and an elevation in Beclin-1; Dex, either alone or combined with ELL, increased Beclin-1, Caspase-3, and P53 expression, which furthered autophagy activity and apoptosis in AMSCs stimulated by Hist and ZDF. covert hepatic encephalopathy Rap's influence was to impede cell viability, augmenting Caspase-3, P53, Beclin-1, and LC3-II/I, while decreasing mTOR and p-mTOR, thereby inducing apoptosis and autophagy; treatment with ELL or ELL along with Dex, however, diminished P53, Beclin-1, and LC3-II/I, thus curbing apoptosis and the excessive autophagy triggered in ASMCs by Rap. Autophagy and cell viability were diminished in the 3-MA model; ELL&Dex considerably increased expression of Beclin-1, P53, and Caspase-3, thereby augmenting apoptosis and autophagy in ASMCs.
ELL in combination with Dex may orchestrate the regulation of ASMC proliferation by triggering apoptosis and autophagy, positioning this combination as a potential medication for asthma.
These results imply that ELL when used with Dex may control the growth of ASMCs by encouraging apoptosis and autophagy, paving the way for a possible treatment for asthma.
The traditional Chinese medicine formula, Bu-Zhong-Yi-Qi-Tang, has held a prominent position in Chinese medicine for more than seven hundred years, treating spleen-qi deficiency, which often leads to issues impacting the gastrointestinal and respiratory systems. Although the bioactive agents orchestrating the restoration of spleen-qi balance remain elusive, many researchers struggle to identify them.
The present study's objective is to evaluate the effectiveness of regulating spleen-qi deficiency, as well as to discover the bioactive compounds in Bu-Zhong-Yi-Qi-Tang.
Bu-Zhong-Yi-Qi-Tang's impact was gauged through blood counts, immune organ sizing, and chemical blood profiles. Structure-based immunogen design Ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry was used to characterize Bu-Zhong-Yi-Qi-Tang prototypes (xenobiotics) in bio-samples and to analyze the potential endogenous biomarkers (endobiotics) in plasma, utilizing metabolomics. By leveraging endobiotics as bait, a network pharmacology approach facilitated the prediction of targets and the identification of potential bioactive components from plasma-absorbed prototypes, culminating in the construction of an endobiotics-targets-xenobiotics association network. Through a poly(IC)-induced pulmonary inflammation mouse model, the anti-inflammatory activities of the representative compounds calycosin and nobiletin were ascertained.
In spleen-qi deficiency rats, Bu-Zhong-Yi-Qi-Tang displayed immunomodulatory and anti-inflammatory activities, as confirmed by increased serum D-xylose and gastrin, a greater thymus size, a higher number of blood lymphocytes, and reduced bronchoalveolar lavage fluid IL-6. Analysis of plasma metabolomics revealed 36 endobiotics associated with Bu-Zhong-Yi-Qi-Tang, principally concentrated in the pathways of primary bile acid biosynthesis, linoleic acid metabolism, and phenylalanine metabolism. Following treatment with Bu-Zhong-Yi-Qi-Tang, the spleen-qi deficiency rat's plasma, urine, small intestinal contents, and tissues were investigated for and found to contain 95 xenobiotics. Six potential bioactive components of Bu-Zhong-Yi-Qi-Tang were examined through the use of an integrated association network. Calcyosin demonstrated a substantial decrease in IL-6 and TNF-alpha levels within the bronchoalveolar lavage fluid, alongside an increase in lymphocyte count, whereas nobiletin notably diminished the concentrations of CXCL10, TNF-alpha, GM-CSF, and IL-6.
A strategy for screening bioactive compounds in BYZQT, designed to address spleen-qi deficiency, was put forth in our investigation, based on the interplay between endobiotics, target molecules, and xenobiotics.
Our study outlined an applicable strategy to screen for bioactive constituents of BYZQT, focusing on spleen-qi deficiency, employing an endobiotics-targets-xenobiotics association network analysis.
China's time-honored Traditional Chinese Medicine (TCM) is slowly but surely garnering greater worldwide appreciation. Chaenomeles speciosa (CSP), a medicinal and edible herb commonly known as mugua in Chinese Pinyin, has been employed in folk medicine for rheumatic diseases, but the precise active components and therapeutic pathways are still being investigated.
We investigate the effects of CSP on inflammation and cartilage protection in rheumatoid arthritis (RA) and the potential targets it interacts with.
An integrated strategy combining network pharmacology, molecular docking, and experimental analysis was undertaken to explore the potential therapeutic mechanism of CSP for cartilage damage associated with rheumatoid arthritis.
Quercetin, ent-epicatechin, and mairin, constituents of CSP, show potential as active compounds for rheumatoid arthritis treatment, targeting AKT1, VEGFA, IL-1, IL-6, and MMP9 as primary targets in a manner supported by molecular docking. In vivo experiments provided confirmation of the potential molecular mechanism proposed by network pharmacology analysis for CSP's treatment of cartilage damage in rheumatoid arthritis. The expression of AKT1, VEGFA, IL-1, IL-6, MMP9, ICAM1, VCAM1, MMP3, MMP13, and TNF- was found to be downregulated by CSP in the joint tissues of Glucose-6-Phosphate Isomerase (G6PI) model mice, which exhibited a concurrent increase in COL-2 expression. CSP plays a role in mitigating rheumatoid arthritis-induced cartilage damage.
Through a multi-pronged approach involving multiple components, targets, and pathways, CSP treatment of cartilage damage in rheumatoid arthritis (RA) demonstrated significant efficacy. It achieved this by suppressing inflammatory markers, reducing neovascularization, diminishing the impact of synovial vascular opacity dissemination, and hindering MMP-mediated cartilage degradation, ultimately safeguarding RA cartilage tissue. Ultimately, this research suggests that CSP might be a promising Chinese medicinal approach for further investigation in the treatment of cartilage damage associated with rheumatoid arthritis.
This investigation of CSP in RA cartilage damage revealed a multi-pronged approach. The treatment's capacity to inhibit inflammatory factor expression, reduce neovascularization, and ameliorate the effects of synovial vascular opacity diffusion, alongside its action to lessen cartilage degradation by matrix metalloproteinases (MMPs), underscores its effectiveness in safeguarding RA cartilage.