Acteoside Counteracts Interleukin‐1β‐Induced Catabolic Processes through the Modulation of Mitogen‐Activated Protein Kinases and the NFκB Cellular Signaling Pathway

Abstract

Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.

Verbascoside Protects Gingival Cells against High Glucose-Induced Oxidative Stress via PKC/HMGB1/RAGE/NFκB Pathway

“…For instance, it has been shown to attenuate the X-rayinduced intracellular ROS and apoptosis in human skin fibroblasts via mitogen-activated protein kinase (MAPK) signaling [34]. Another study demonstrated that verbascoside inhibited various inflammatory mediators in the primary rat chondrocytes treated with IL-1β through the MAPK pathway as well [35]. Moreover, recent studies have suggested verbascoside possessed the anti-diabetic potential since it has been reported to lower hyperglycemia and hyperlipidemia in diet/STZ-induced diabetic rats [36].…”

The Neuroprotection of Verbascoside in Alzheimer’s Disease Mediated through Mitigation of Neuroinflammation via Blocking NF-κB-p65 Signaling

“…In a 12 h light/dark cycle, free access to food and water were offered to all mice. APP/PS1 mice were stochastically assigned to two groups: (i) the model group that was orally treated with 0.4 mL of normal saline ( n = 12) daily for 6 weeks and (ii) the VB-treated group that was orally treated during the same period with 10 mg/kg of VB (61276-17-3, 98.38% purity, Chengdu Herbpurify Co., Ltd., Chengdu, China), which was firstly dissolved with DMSO (1/2000 V total ) before diluting with normal saline ( n = 12) [ 23 , 24 ]. WT mice ( n = 12) were administered 0.4 mL of normal saline daily for 6 weeks through the gastric route and served as the control group.…”

The pharmacokinetic property and pharmacological activity of acteoside: A review

“… [121] Bone and cartilage protection Rats Inhibits MMP-13, MMP-3, and MMP-1 expression by decreasing MAPK/NF-κB signaling. [19] Mice Reduces osteoclastogenesis by attenuation of NF-κB pathway and stimulation of PI3K/AKT pathway. [125] MC3T3-E1 Enhances proliferation and differentiation by increasing IGF-1/BMP/PI3K/mTOR signaling [127] …”

“…In addition, Srivastava also discusses some pharmacological activities of AC [12] . From the sophisticate literature research, we find that AC has been reported various pharmacological activities, including anti-oxidation [14] , anti-inflammation [15] , anti-cancer [11] , neuroprotection [16] , cardiovascular protection [17] , anti-diabetes [18] , bone and cartilage protection [19] , hepatoprotection [20] , and anti-microorganism [21] . In this review, we will mainly focus on these fields and summarize the research progress of AC, including the pharmacokinetic profiles.…”