Protective Effect Of Aucubin Research Articles

Traditional Chinese Medicine formula Bu-Shen-Huo-Xue-Fang (BSHXF) protects nucleus pulposus cells against the inflammatory and oxidative stress-induced degenerative changes

Degeneration of the intervertebral disc is primarily caused by the loss of nucleus pulposus cells (NPCs) and extracellular matrix (ECM) (IDD). Bu-Shen-Huo-Xue-Fang (BSHXF), a traditional Chinese medicine decoction, has been used to treat IDD in clinical; nevertheless, the active components and underlying molecular mechanisms remain unknown. BSHXF improved IL-1β and H2O2 stimulation-induced injuries on NPCs by promoting cell viability, increasing ECM deposition, inhibiting cell senescence, and decreasing the levels of inflammatory factors. The active ingredients in BSHXF were identified by LC-MS/MS analysis; three active ingredients from the principal drugs, Aucubin, Tanshinol, and Tanshinone II A promoted NPC viability; and Aucubin and Tanshinol promoted NPC viability more. Aucubin and Tanshinol, respectively, improved H2O2 stimulation-induced injuries on NPCs by promoting cell viability, increasing ECM deposition, inhibiting cell senescence, and decreasing the levels of inflammatory factors. The activator of NF-κB and Wnt signaling pathways attenuated Aucubin and Tanshinol's protective effects by promoting ECM degradation and NPC senescence. Aucubin, Tanshinol, and Tanshinone II A were identified as the most potent compounds in BSHXF protection against degenerative changes in NPCs. The NF-κB and Wnt signaling pathways might be involved in the protective effects of Aucubin and Tanshinol against H2O2-induced degenerative changes.

Protective effects of aucubin against nonylphenol-induced liver toxicity by improving biochemical, inflammatory and histopathological indices

Nonylphenol (NP) is a ubiquitous environmental toxicant that is known to cause hepatotoxicity via generation of reactive oxygen species (ROS). Aucubin (AUC), an iridoid glucoside, is a potential phytochemical possessing antioxidant and anti-inflammatory features. The current study was intended to ascertain the hepatoprotective role of AUC against NP-generated liver toxicity in rats. 48 male rats were distributed into four groups. viz. Control, NP-intoxicated group (50 mg/kg), NP + AUC-treated group (50 mg/kg + 40 mg/kg) and AUC-treated group (40 mg/kg). All the doses were administered orally. Our findings indicated that the NP intoxication upregulated the alanine aminotransferase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) level. Moreover, it brought down the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GSR) and glutathione-S-transferase (GST), as well as the glutathione (GSH) content. Conversely, the levels of malondialdehyde (MDA) and ROS were escalated. Besides, the levels of nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 as well as the cyclooxygenase-2 (COX-2) activity were elevated due to the NP administration. In addition to it, histopathological assessment displayed the prominent morphological alterations in hepatic tissues of rats. Nevertheless, treating the rats with AUC significantly (p < 0.05) abated all the NP-instigated liver damages in rats. Therefore, it was evinced that AUC could be used as a hepatoprotective agent against the NP-prompted liver toxicity owing to its antioxidant and anti-inflammatory properties.

Protective effect of aucubinon on the eucommia ulmoides on skin photoaging induced by UVB

Objective To explore the protective effect of aucubin on the photoageing of the skin that induced by ultraviolet (UVB) radiation. Methods Human skin fibroblasts were divided into normal group, model group and high, medium and low dose groups of apocynin by random method. Except the normal group, the other groups of cells were subjected to UVB radiation with a radiation wavelength of 311 nm, irradiation intensity of 9.00 mw/cm2, radiation time of 2.8 s, radiation dose of 25 mJ/cm2. The cells in the high, medium and low doses of aglycone were cultured for 24 h at an equal volume of 400, 200, 100 μg/ml, and then subjected to UVB irradiation, and then cultured for 24 h. The normal group and the model group were cultured for 48 h in a common medium. The apoptosis rate of each group was detected by flow cytometry. The levels of IL-1, IL-6 and TNF-α in each group were detected by ELISA. The expressions of Bax and Bcl-2 mRNA in each group were detected by RT-PCR. Results Compared with the model group, the apoptosis rate (4.84% ± 0.24%, 12.32% ± 0.67% vs. 35.63% ± 2.77%) in the medium and high dose group significantly decreased (P<0.05), the content of IL-1 (21.14 ± 1.94 ng/ml, 16.17 ± 0.74 ng/ml vs. 22.55 ± 1.02 ng/ml), IL-6 (17.46 ± 0.93 ng/ml, 14.51 ± 0.79 ng/ml vs. 18.39 ± 2.05 ng/ml), TNF-α (44.21 ± 1.16 ng/ml, 35.94 ± 3.08 ng/ml vs. 45.67 ± 2.28 ng/ml) significantly increased (P<0.05). Compared with the model group, the expression of Bax mRNA (0.29 ± 0.05, 0.42 ± 0.05, 0.51 ± 0.04 vs. 0.59 ± 0.05) significantly decreased, and the expression of Bcl-2 mRNA (0.52 ± 0.04, 0.44 ± 0.03, 0.35 ± 0.03 vs. 0.26 ± 0.04) significantly increased (P<0.05). Conclusions The aucubin has protective function to the damage of skin fibroblasts which is induced by UVB radiation, indicating the protective function of decreasing Bax mRNA expression, increasing Bcl-2 mRNA expression, reducing the expression of inflammatory factor IL-1, IL-6, TNF-α, holding-up the cell apoptosis which is induced by UVB radiation, and inhibiting apoptosis of cell that caused by UVB radiation, playing an role of protective fibroblasts for delay of the photoageing. Key words: Eucommiae cortex; Aucubin; Ultraviolet rays; Apoptosis; Skin care; Fibroblasts

Protective effects of aucubin on osteoarthritic chondrocyte model induced by hydrogen peroxide and mechanical stimulus

BackgroundDuring the onset of osteoarthritis (OA), certain biochemical events have been shown to accelerate cartilage degradation, including the dysregulation of cartilage ECM anabolism, abnormal generation of reactive oxygen species (ROS) and overproduction of proteolytic enzymes and inflammatory cytokines. The potency of aucubin in protecting cellular components against oxidative stress, inflammation and apoptosis effects are well documented, which makes it a potential candidate for OA treatment. In this study, we aimed to evaluate the protective benefits of aucubin against OA using H2O2 and compression induced OA-like chondrocyte models.MethodsThe effects of aucubin were studied in porcine chondrocytes after 1 mM H2O2 stimulation for 30 min or sustained compression for 24 h. Effects of aucubin on cell proliferation and cytotoxicity of chondrocytes were measured with WST-1 and LDH assays. ROS production was evaluated by the Total ROS/Superoxide Detection Kit. Caspase-3 activity was evaluated by the CaspACE assay system. The levels of apoptosis were evaluated by the Annexin V-FITC apoptosis detection kit. OA-related gene expression was measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Total DNA quantification was evaluated by the DNeasy Blood and Tissue kit. Sulfated-glycosaminoglycans (sGAGs) production and content were evaluated by DMMB assay and Alcian blue staining.ResultsThe results showed that the ROS scavenge effects of aucubin appeared after 1 h of pretreatment. Aucubin could reduce the caspase-3 activity induced by H2O2, and reduced the apoptosis cell population in flowcytometry. In RT-qPCR results, aucubin could maintain ACAN and COL2A1 gene expressions, and prevent IL6 and MMP13 gene up-regulation induced by H2O2 and compression stimulations. In the DMMB assay and Alcian blue staining, aucubin could maintain the sGAG content and protect chondrocytes against compressive stress, but not oxidative stress from H2O2.ConclusionsThese results indicated that aucubin has protective effects in an osteoarthritic chondrocyte model induced by H2O2 and mechanical stimulus.