Search

A number of studies demonstrated that some tea extracts exert inhibitory effects on osteoclastogenesis induced by receptor activator of nuclear factor κB ligand (RANKL). However, the effect of purple tea, a famous tea in China, on osteoclastogenesis remains unclear. In this study, a water-based purple tea extract (PTE) was found to suppress osteoclast formation, osteoclastic resorption pit area formation, and F-actin ring formation within RANKL-stimulated bone marrow macrophages (BMMs). Furthermore, our results demonstrated that PTE could inhibit expression of master transcription factors NFATc1 and c-Fos and their target genes

The effects of ginseng oligosaccharides (GSOs) on neuronal oxidative injury induced by glutamate (GLU) and the molecular mechanisms involved were investigated. Cell damage was assessed using MTT assays, and the lactate dehydrogenase (LDH) release rate and flow cytometry were used to detect the accumulation of reactive oxygen species (ROS) and mitochondrial membrane potential respectively. The levels of catalase (CAT) and glutathione (GSH) were measured in PC12 cells and Drosophila brain tissue. The climbing ability of Drosophila was observed. Levels of proteins, including Cyt C, Bcl-2/BAX, and Nrf2/HO-1-associated proteins, were determined by western blotting and immunofluorescence. It was found that GSOs reversed GLU-induced reductions in cell viability and the LDH release rate, and rescued ROS accumulation. GSOs also mitigated the deleterious effects of GLU on the mitochondrial membrane potential and Cyt C release, thus alleviating mitochondrial dysfunction, and increased GSH levels and CAT activity in both cells and Drosophila brain tissue. The climbing index in GSO-treated Drosophila was significantly higher than that in the

Chronically elevated free fatty acid levels can adversely affect pancreatic β-cells, leading to insulin resistance and eventually type 2 diabetes mellitus (T2DM). Polydatin (PD) from Polygonum cuspidatum has been shown to regulate blood lipid content and lower cholesterol levels. However, there have been no reports on the potential therapeutic effects and actions of PD on lipotoxicity in β-cells.This study aimed to investigate the protective effects of PD on palmitate (PA)-treated INS-1 insulinoma cells and diabetic mice.Cells were incubated with PA and varying concentrations of PD for 24 h. Viability assays, morphological observations, flow cytometric analysis, western blotting, and reverse transcription-quantitative polymerase chain reaction were used to assess the effects of PD on PA-induced lipotoxicity. Western blotting was used to measure the endoplasmic reticulum stress (ERS) and the levels of autophagy-related factors after incubation with inducers and inhibitors of ERS and autophagy. Diabetic mice were treated with intragastric PD for 6 weeks followed by the measurement of their physiological and blood lipid indices and assessment of the results of histological and immunofluorescence analyses.Treatment with PD after PA exposure enhanced insulin secretion and the expression of diabetes-associated genes. PD promoted β-cell function by reducing the levels of proteins associated with ERS and autophagy while also attenuating ERS triggered by tunicamycin. PD also reduced tunicamycin-induced autophagy, indicating that it regulated ERS-mediated autophagy and reduced PA-induced cellular dysfunction. In addition, treatment of db/db mice with PD substantially reduced body weight gain, alleviated dyslipidemia, improved β-cell function, and reduced insulin resistance.These results suggest that PD protects β-cells from lipotoxicity-induced dysfunction and apoptosis by inhibiting ERS and preventing excessive autophagy. Our study provides a new basis for exploring the potential of PD against β-cell lipotoxicity and T2DM.

Aerobic cellular respiration provides chemical energy, adenosine triphosphate (ATP), to maintain multiple cellular functions. Sirtuin 1 (SIRT1) can deacetylate peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) to promote mitochondrial biosynthesis. Targeting energy metabolism is a potential strategy for the prevention and treatment of various diseases, such as cardiac and neurological disorders. Ginsenosides, one of the major bioactive constituents ofIn this study, oxygen consumption rate, ATP production, mitochondrial biosynthesis, glucose metabolism, and SIRT1-PGC-1α pathways in untreated and GS-treated different cells, fly, and mouse models were investigated.GS pretreatment enhanced mitochondrial respiration capacity and ATP production in aerobic respiration-dominated cardiomyocytes and neurons, and promoted tricarboxylic acid metabolism in cardiomyocytes. Moreover, GS clearly enhanced NADThis study may provide new insights into the extensive application of ginseng for cardiac and neurological protection in healthy subjects and patients.

Spectroscopic analysis of HPLC-purified 7.3-kD Acorus tatarinowii Schott root polysaccharide ASP2-1 (FT-IR, NMR) revealed respective monosaccharide proportions of glucose: galactose: arabinose: xylose: galacturonic acid: mannose: rhamnose: glucuronic acid:fucose of 49.1:16.0:11.6:10.2:5.3:2.9:2.2:1.7:0.8. In vitro, ASP2-1 inhibited osteoclastogenesis-associated bone resorption, RANKL-induced osteoclastogenesis and F-actin ring formation and suppressed osteoclastogenesis-associated gene expression (e.g., TRAP, OSCAR, Atp6v0d2, αV, β3, MMP9 and CtsK) as shown via RT-PCR. ASP2-1-treated RANKL-stimulated bone marrow-derived macrophages exhibited decreased levels of NFATc1 and c-Fos mRNAs and corresponding transcription factor proteins, elevated expression of negative NFATc1 regulators (Mafb, IRF8, Bcl6) and reduced their upstream negative regulator (Blimp1) expression. ASP2-1 inhibition of NFATc1 expression involved PLCγ2-Ca2+ oscillation-calcineurin axis suppression, reflecting suppression of RANKL-induced PLCγ2 activation (and associated Ca2+ oscillation) and calcineurin catalytic subunit PP2BAα expression without inhibiting NF-κB and MAPKs activation or phosphorylation. Staining (H&E, TRAP) and micro-CT assays revealed ASP2-1 attenuated bone destruction and osteoclast over-activation and improved tibia micro-architecture in a murine LPS-induced bone loss model. Thus, ASP2-1 may alleviate inflammatory bone loss-associated diseases.

Ethnopharmacological relevance Skin barrier dysfunction can lead to water and electrolyte loss, triggering homeostatic imbalances that can trigger atopic dermatitis and anaphylaxis. Panax ginseng C.A. Meyer is a traditional Chinese medicinal herb with known therapeutic benefits for the treatment of skin diseases, including photodamage repair effects and reduction of pigmentation. However, few reports exist that describe effectiveness of ginseng active components for repair of skin barrier damage. Materials and methods Ginseng oligosaccharide extract (GSO) was prepared from P. ginseng via water extraction followed by ethanol precipitation and resin and gel purification. GSO composition and structural characteristics were determined using LC-MS, HPLC, FT-IR, and NMR. To evaluate GSO as a skin barrier repair-promoting treatment, skin of UVB-irradiated BALB/c hairless mice was treated with or without GSO then skin samples were evaluated for epidermal thickness, transepidermal water loss (TEWL), and stratum corneum water content. In addition, UVB-exposed skin samples and HaCaT cells were analyzed to assess GSO treatment effects on levels of epidermal cornified envelope (CE) protein and other skin barrier proteins, such as filaggrin (FLG), involucrin (IVL), and aquaporin-3 (AQP3). Meanwhile, GSO treatment was also evaluated for effects on UVB-irradiated hairless mouse skin and HaCaT cells based on levels of serine protease inhibitor Kazal type-5 (SPINK5), trypsin-like kallikrein-related peptidase 5 (KLK5), chymotrypsin-like KLK7, and desmoglein 1 (DSG1). These proteins are associated with UVB-induced skin barrier damage manifesting as dryness and desquamation. Results GSO was shown to consist of oligosaccharides comprised of seven distinct types of monosaccharides with molecular weights of approximately 1 kDa that were covalently linked together via β-glycosidic bonds. In vivo, GSO applied to dorsal skin of BALB/c hairless mice attenuated UVB-induced epidermal thickening and moisture loss. Furthermore, GSO ameliorated UVB-induced reductions of levels of FLG, IVL, and AQP3 proteins. Additionally, GSO treatment led to increased DSG1 protein levels due to decreased expression of KLK7. In vitro, GSO treatment of UVB-irradiated HaCaT cells led to increases of FLG, IVL, and AQP3 mRNA levels and corresponding proteins, while mRNA levels of desquamation-related proteins SPINK5, KLK5, KLK7, and DSG1 and associated protein levels were restored to normal levels. Conclusion A P. ginseng oligosaccharide preparation repaired UVB-induced skin barrier damage by alleviating skin dryness and desquamation symptoms, highlighting its potential as a natural cosmetic additive that can promote skin barrier repair after UVB exposure.

Aims Oxygen and glucose deprivation and reperfusion (OGD/R) injury contributes to the pathophysiology after ischemic stroke, which needs to urgently develop treatment strategies. Previous studies have demonstrated that autophagy in reperfusion period exerted adverse effects on the cerebral ischemic injury. Ginsenoside monomer compound K (CK) is the main intestinal metabolite of ginseng that exerts the pharmacological activities and has a protective effect against cerebral OGD/R injury. However, the specific molecular mechanism of CK protects against OGD/R injury in neurons is still unclear. Materials and methods In this study, cell viability, reactive oxygen species (ROS) generation, Ca2+ overload, mitochondrial membrane potential depolarization, autophagy and apoptosis were investigated in OGD/R-induced neuronal cells injury after pretreatment with CK and in combination with BML-275 or rapamycin. Key findings Our study found that pretreatment with CK protected neurons against OGD/R injury by increasing cell viability and decreasing the ROS generation, mitochondrial damage, and Ca2+ overload. Moreover, CK cut down autophagy-mediated apoptosis via promoting the process of forming autophagosomes into phagocytic precursors. Furthermore, our study clarified the neuroprotective of CK against OGD/R-induced neural autophagy and apoptosis through the regulation of the AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) pathway. Significance Taken together, our study provides credible experimental evidence and explains the potential molecular mechanism of CK as one of the main bioactive ingredients of ginseng for the treatment of cerebral ischemia/reperfusion injury.