Ruscogenin, a steroidal sapogenin, is primarily derived from the genus Ruscus. It demonstrates a wide range of pharmacological actions that hold substantial promise for therapeutic use. By conducting a comprehensive examination of electronic databases including PubMed, ScienceDirect, and SciFinder, we identified studies on ruscogenin to date. This review aims at emphasizing the findings related to the bioactivities of ruscogenin, particularly its protective activities in neurological and inflammatory disorders, hemorrhoids, and cancer. Ruscogenin has been demonstrated to possess anti-ulcer, anti-osteoporotic, and skin-lightening properties as a therapeutic agent. It has also been proven effective in managing metabolic disorders by reducing inflammation and improving lipid metabolism, particularly in conditions such as non-alcoholic steatohepatitis and diabetic nephropathy. Reports indicate that it can prevent acute lung injury by protecting pulmonary endothelial cells from apoptosis and modulating inflammatory cytokines. Additionally, ruscogenin promotes neurological recovery by mitigating oxidative stress. It also shows anti-cancer properties, leading to apoptosis and hindering metastasis, particularly in pancreatic and hepatocellular carcinoma. This review summarizes the potential medical applications of ruscogenin and underscores the need for further research on its mechanisms of action.
Objective: To investigate the antifibrotic effects of curcumin in a transverse aortic constriction (TAC) mouse model and elucidate its molecular mechanisms.
Methods: Male C57BL/6 mice underwent TAC and received vehicle, low-dose curcumin (50 mg/kg), high-dose curcumin (200 mg/kg), high-dose curcumin plus a scrambled control antagomir, or high-dose curcumin plus anti-miR-29b treatments. Cardiac function was assessed by echocardiography. Fibrosis was evaluated by histology, collagen volume fraction, and hydroxyproline content. Expression of miR-29b, HDAC4, and fibrosis-related markers (Collai, Col3a1, TGF-β1) was measured by quantitative RT-PCR and Western blotting assays. Myocardial procollagen type I carboxyterminal propeptide was determined by ELISA, and HDAC4-specific enzymatic activity was assayed using a fluorogenic kit.
Results: Curcumin improved cardiac function, reduced fibrosis, restored miR-29b expression, and suppressed HDAC4 expression and activity in a dose-dependent manner. Furthermore, curcumin decreased myocardial procollagen type I carboxy-terminal propeptide levels, confirming reduced collagen synthesis. Anti-miR-29b administration partially abrogated the antifibrotic and cardioprotective effects of curcumin.
Conclusions: Curcumin attenuates pressure overload-induced cardiac fibrosis and dysfunction in a TAC mouse model via modulation of the miR-29b/HDAC4 axis and suppression of collagen synthesis.
Objective: To evaluate the effects of a piceatannol-loaded self-nanoemulsifying drug delivery system (PIC-SNEDDS) on wound healing in diabetic rats and its mechanisms of wound healing action.
Methods: Diabetes was induced in rats using streptozotocin, after which full-thickness excisional wounds were created. Piceatannol was administered topically either as a raw hydrogel or formulated into a PIC-SNEDDS, which was prepared using an optimized oil-surfactant mixture and incorporated into a hydrogel for application. Wound healing activity was assessed through measurements of wound contraction, oxidative stress biomarkers, and collagen content, along with histological and immunohistochemical evaluation of inflammatory, angiogenic, and remodeling markers.
Results: PIC-SNEDDS markedly enhanced diabetic wound healing by promoting epithelial regeneration, granulation tissue formation, epidermal proliferation, and keratinization. The formulation also reduced the expression of pro-inflammatory markers (interleukin-6, nuclear factor-kappa B, and tumor necrosis factor-α) while increasing α-smooth muscle actin, transforming growth factor-β1, vascular endothelial growth factor-A, and hydroxyproline levels. Additionally, it improved antioxidant status by lowering malondialdehyde levels and boosting superoxide dismutase and catalase activity, along with upregulation of COL1A1 mRNA expression.
Conclusions: PIC-SNEDDS promotes the healing of diabetic wounds and exhibits anti-inflammatory, antioxidant, pro-collagen, and angiogenic properties.
Objective: To investigate the anti-atherosclerosis effect of chikusetsusaponin IV (CSIV) against high-fat diet-induced atherosclerosis in rats.
Methods: A high-fat diet was used for the induction of atherosclerosis in rats, and the rats received oral CSV or atorvastatin. The body weight, organ weights, food intake, calorie intake, lipid parameters, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)/mevalonate ratio, collagen, free fatty acid, cardiac parameters, apolipoprotein (A and B), antioxidant parameters, inflammatory cytokines, and inflammatory parameters were assessed. The mRNA expressions of interleukin-1β (IL-β), tumor necrosis factor-α (TNF-α), IL-6, IL-17, PI3K, AKT, and mTOR were estimated.
Results: CSV significantly modulated food intake, body weight, organ weight (liver, kidney, and heart), and calories (P<0.05). Total cholesterol, triglycerides, very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol, cardiovascular risk index-1, and cardiovascular risk index-2 were decreased, while high-density lipoprotein cholesterol and anti-atherogenic index were increased significantly in the CSV group (P<0.05). Besides, CSV significantly restored the level of HMG-CoA/mevalonate ratio, collagen, free fatty acid, cardiac parameters (creatinine kinase-MB, lactate dehydrogenase, cTnT, cTnI), apolipoprotein (apolipoprotein A and apolipoprotein B), antioxidant parameters (MDA, CAT, GPx, GSH, SOD), inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-10), inflammatory parameters (COX-2, TGF-β, NF-κB), intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1. CSV also decreased the mRNA expression of IL-1β, TNF-α, IL-6, IL-17, PI3K, AKT, and mTOR.
Conclusions: This study showed the anti-atherosclerosis effect of CSV against high-fat diet-induced atherosclerosis in rats via alteration of NF-κB/COX-2 and PI3K/AKT/mTOR signaling pathway.
Objective: To investigate the effect of Catalpa ovata fruit extract (COFE) on muscle growth and exercise performance in C2C12 myoblasts and mice.
Methods: Cell viability was determined through a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Myogenic differentiation was observed using Giemsa staining. COFE was administered to mice orally at 50 and 200 mg/kg for 10 weeks. Muscular strength was evaluated using the whole-limb grip strength assay. The expression levels of myogenesis- and energy metabolism-related proteins in vitro and in vivo were determined using Western blotting.
Results: COFE significantly improved myoblast-to-myotube differentiation in C2C12 myoblasts. It also increased the expression of myogenesis determination protein 1 and myogenin compared with the control group. Moreover, the expression levels of glucose transporter type 4 (Glut4) and peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) were significantly elevated in the presence of COFE in C2C12 myoblasts. COFE also markedly increased phosphorylation of AMP-activated protein kinase, which regulates Glut4 and POC-1α expression levels in C2C12 myoblasts. Mice treated with COFE showed improved grip strength. Myogenesis- and energy metabolism-related protein levels in muscle tissue were significantly increased in COFE-administered mice.
Conclusions: COFE treatment improves exercise performance by controlling myogenesis and energy metabolism in skeletal muscle. COFE has the potential to be used as an effective natural agent for enhancing muscular strength.