akebia-saponin-d and Inflammation

Gestational diabetes mellitus (GDM) is a prevalent and severe metabolic disease in pregnant women that is characterized by a high incidence. Placental oxidative stress and inflammation are recognized as the primary contributors to GDM pathogenesis. The repressive effect of akebia saponin D (ASD) on oxidative stress and inflammation has been demonstrated in various diseases.. To investigate the impact of ASD on GDM.. Animal experimental study.. GDM mice were intraperitoneally treated with ASD. The effect of ASD on GDM symptoms, blood lipid levels, pancreatic tissue damage, gestational outcomes, oxidative stress, and inflammation was assessed via intraperitoneal glucose and insulin tolerance tests, serum glucose and insulin level determination, lipid biochemistry analysis, pathological staining, oxidative stress evaluation, western blot analysis, and enzyme-linked immunosorbent assay.. ASD reduced the GDM-induced increase in body weight and blood glucose levels while restoring the decreased insulin levels associated with GDM. In addition, ASD improved the serum lipid parameters, pancreatic tissue damage, and gestational outcomes in GDM mice. Furthermore, ASD reversed the decreased levels of superoxide dismutase and glutathione while reducing the elevated concentrations of malondialdehyde and myeloperoxidase in GDM mice. In addition, ASD rescued the relative protein expression of nuclear factor-E2-related factor 2 and heme oxygenase-1 in the placenta of GDM mice. Additionally, ASD counteracted the increase in tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels in the sera and placenta of GDM mice.. ASD suppressed oxidative stress and inflammation to effectively relieve symptoms and gestational outcomes of the GDM mice.

Topics: Animals; Diabetes, Gestational; Female; Glucose; Humans; Inflammation; Insulins; Mice; Placenta; Pregnancy; Pregnancy Outcome

Akebia saponin D (ASD) is derived from the

Topics: Anti-Inflammatory Agents; Dinoprostone; DNA; Humans; Inflammation; Inflammation Mediators; Interleukin-6; Lipopolysaccharides; Methyltransferases; NF-E2-Related Factor 2; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; RNA, Messenger; RNA, Small Interfering; Saponins; STAT3 Transcription Factor; Tumor Necrosis Factor-alpha

Diabetic nephropathy (DN), a common microvascular complication of type 2 diabetes mellitus (T2DM), causes increasing mortality and morbidity due to its high prevalence and severe consequences. Hence, it is urgent to search for effective agents that provide new insights into novel molecular therapeutic targets for DN. This study was designed to investigate the critical role of Akebia saponin D (ASD) in kidney damage, inflammation and apoptosis of renal tubular cells in DN. To probe the protective effects of ASD on DN in vivo, diabetes mellitus model was established by intraperitoneal (ip) injection of STZ (60 mg/kg) for 5 days consecutively. Besides, HG-induced human renal tubular cells (HK-2) were used to analyze the defined effects and underlying mechanism of ASD on DN in vitro. Blood glucose, insulin, serum creatinine (Scr), blood urea nitrogen (BUN), renal injury, inflammation, oxidative stress and apoptosis of renal tubular cells were respectively measured and evaluated. ASD prevented kidney damage, improved renal function and inflammatory reaction, ameliorated oxidative stress and inhibited apoptosis of renal tubular cells in DN mice via activation of NRF2/HO-1 pathway and inhibition of NF-KB pathway.

Topics: Acute Kidney Injury; Animals; Anti-Inflammatory Agents; Apoptosis; Cell Line; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Epithelial Cells; Humans; Inflammation; Kidney; Male; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; NF-kappa B; Oxidative Stress; Saponins; Signal Transduction

As an ordinary joint vestigial disease, osteoarthritis (OA) contributes to a considerable proportion of disability cases worldwide. Inflammation, as the main pathological factor, mediates the occurrence and development of OA. Akebia Saponin D (ASD), also known as Asperosaponin VI, is one of the active components extracted from Dipsaci Radix and is rich in Dipsacus loose tea. It has shown sound therapeutic effects on various diseases; nevertheless, its role in OA therapy is not completely understood. This study demonstrated the anti-inflammatory activity of ASD in OA through a series of in vivo and in vitro experiments. In vitro experiments revealed that ASD might prohibit the production of inflammatory mediators in IL-1β treated chondrocytes such as COX-2, iNOS, NO, PGE2, IL-6, and TNF-α. Meanwhile, it may also inhibit the production of ADAMTS-5 and MMP13 and promote the production of Aggrecan and Collagen II. The mechanism study demonstrated that ASD exerted an anti-inflammatory effect by activating the NRF2 target, upregulating the expression of HO-1, and preventing P65 from binding to DNA. In vivo experiments demonstrated that ASD might improve the progression of OA in a DMM mouse model. These research results provide evidence for the potential application of ASD in OA therapy.

Topics: Animals; Anti-Inflammatory Agents; Chondrocytes; Cyclooxygenase 2; Female; Heme Oxygenase (Decyclizing); Inflammation; Inflammation Mediators; Interleukin-1beta; Male; Matrix Metalloproteinase 13; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; NF-kappa B; Nitric Oxide Synthase Type II; Osteoarthritis; Saponins

Neuroinflammatory responses caused by amyloid β(Aβ) play an important role in the pathogenesis of Alzheimer's disease (AD). Aβ is known to be directly responsible for the activation of glial cells and induction of apoptosis. Akebia Saponin D (ASD) is extracted from a traditional herbal medicine Dipsacus asper Wall, which has been shown to protect against ibotenic acid-induced cognitive deficits and cell death in rats. In this study, we investigated the in vivo protective effect of ASD on learning and memory impairment induced by bilateral intracerebroventricular injections of Aβ1-42 using Morris water and Y-maze task. Furthermore, the anti-inflammatory activity and neuroprotective effect of ASD was examined with methods of histochemistry and biochemistry. These data showed that oral gavage with ASD at doses of 30, 90 and 270 mg/kg for 4 weeks exerted an improved effect on cognitive impairment. Subsequently, the ASD inhibited the activation of glial cells and the expression of tumor necrosis factor (TNF)-α, interleukin-1 beta (IL-1β) and cyclooxygenase-2 (COX-2) in rat brain. Moreover, ASD afforded beneficial actions on inhibitions of Akt and IκB kinase (IKK) phosphorylations, as well as nuclear factor κB (NF-κB) activation induced by Aβ1-42. These results suggest that ASD may be a potential agent for suppressing both Alzheimer's disease-related neuroinflammation and memory system dysfunction.

Topics: Amyloid beta-Peptides; Animals; Cognition Disorders; Cytokines; Disease Models, Animal; Drug Administration Routes; Gene Expression Regulation; Glial Fibrillary Acidic Protein; Hippocampus; Inflammation; Male; Maze Learning; NF-kappa B p52 Subunit; Oncogene Protein v-akt; Peptide Fragments; Phosphorylation; Rats; Rats, Sprague-Dawley; Saponins; Signal Transduction