Astilbin ameliorates cisplatin-induced nephrotoxicity through reducing oxidative stress and inflammation.
Wang Si-Wei,Xu Yi,Weng Yuan-Yuan,Fan Xue-Yu,Bai Yong-Feng,Zheng Xiao-Yan,Lou Li-Jun,Zhang Feng
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
Oxidative stress and inflammation are considered to be the main pathogenesis of cisplatin nephrotoxicity. Astilbin, a flavonoid with anti-oxidation and anti-inflammation function, has been used to treat heavy metal induced kidney injury. In this study, we investigated the protective effects of astilbin on cisplatin-induced nephrotoxicity and its underlying mechanisms. Our results showed that astilbin markedly inhibited cisplatin-induced cell apoptosis and recovered cell growth. Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293 cell apoptosis. Astilbin effectively enhanced NRF2 activation and transcription of its targeting antioxidant genes to reduce ROS accumulation in cisplatin-induced HEK-293 cells. Furthermore, we found that astilbin obviously suppressed tumor necrosis factor alpha (TNF-α) expression and NF-κB activation, and also inhibited the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Finally, we confirmed that the effect of astilbin to improve renal oxidative stress and inflammation in cisplatin induced acute nephrotoxic mice. In conclusion, our study suggests that astilbin could ameliorate the cisplatin-induced nephrotoxicity by reducing oxidative stress and inflammation.
Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells.
Chen Fang,Zhu Xiaoguang,Sun Zhiqiang,Ma Yali
Frontiers in pharmacology
Diabetic nephropathy (DN) is characterized by inflammatory responses and extracellular matrix (ECM) accumulation. Astilbin is an active natural compound and possesses anti-inflammatory activity. The aim of this study was to evaluate the anti-inflammatory effect of astilbin on high glucose (HG)-induced glomerular mesangial cells and the potential mechanisms. The results showed that HG induced cell proliferation of HBZY-1 cells in a time-dependent manner, and astilbin inhibited HG-induced cell proliferation. The expression and secretion of inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and ECM components, including collagen IV (Col IV) and fibronectin (FN), were induced by HG. Moreover, TGF-β1 and CTGF were also induced by HG. The induction by HG on inflammatory response and ECM accumulation was inhibited after astilbin treatment. Astilbin treatment also attenuated HG-induced decrease in expression of matrix metalloproteinase (MMP)-2 and MMP-9. The TLR4/MyD88/NF-κB pathway was activated by HG, and the inhibitor of TLR4 exhibited the same effect to astilbin on reversing the induction of HG. TLR4 overexpression attenuated the effect of astilbin on HG-induced inflammatory cytokine production and ECM accumulation. The results suggested that astilbin attenuated inflammation and ECM accumulation in HG-induced rat glomerular mesangial cells via inhibiting the TLR4/MyD88/NF-κB pathway. This work provided evidence that astilbin can be considered as a potential candidate for DN therapy.
Protective effects of Rhizoma smilacis glabrae extracts on potassium oxonate- and monosodium urate-induced hyperuricemia and gout in mice.
Liang Guoyan,Nie Yichu,Chang Yunbing,Zeng Shixing,Liang Changxiang,Zheng Xiaoqing,Xiao Dan,Zhan Shiqiang,Zheng Qiujian
Phytomedicine : international journal of phytotherapy and phytopharmacology
BACKGROUND:Rhizoma smilacis glabrae (RSG, tufuling) has been widely used in traditional Chinese medicine for deoxidation, dampness relief, and easing joint movement. The chemical composition of RSG has been systematically confirmed, and some of its compounds have been revealed to possess antioxidant, anti-inflammatory, immunomodulatory, hypouricemic, and hepatoprotective effects. PURPOSE:We aimed to clarify whether a RSG extract attenuates hyperuricemia, paw edema, and renal injury in mice with potassium oxonate (PO)- and monosodium urate (MSU)-induced chronic hyperuricemia and gout. METHODS:RSG water extract was obtained and analyzed by HPLC-DAD-MS/MS. To establish a murine model with chronic hyperuricemia and gout, PO was orally administered daily from day 0 to day 24, whereas MSU was injected into the tibiotarsal joint on day 21. The mice in the drug intervention groups were treated once daily with doses of allopurinol or RSG extract from day 21 to day 24. The diameter of the ankle joints was measured with calipers. Serum TNF-α and IL-1β concentrations, hepatic XOD activity, and uric acid, creatinine, and blood urea nitrogen (BUN) levels were also determined. The right kidney and articular cavities were fixed, cut into sections, and stained with hematoxylin and eosin. RESULTS:Nine compounds in the RSG water extract were unambiguously identified as 5-O-caffeoylshikimic acid, neoastilbin, astilbin, taxifolin, neoisoastilbin, isoastilbin, engeletin, isoengeletin, and trans-resveratrol. The RSGE treatment dose-dependently reduced PO- and MSU-induced paw edema, serum TNF-α, IL-1β, IL-6, IL-12, uric acid, and BUN, while significantly elevated serum IL-10, urinary uric acid and creatinine levels as compared with the respective values in the hyperuricemic and gouty mice group (vehicle group). Moreover, the hepatic XOD activity was dose-dependently reduced by the RSGE treatment. In addition, RSGE treatment not only ameliorated the infiltration of inflammatory cells, tubular dilation and vacuole formation in renal tubular, but also improved the synovial hyperplasia, reduced inflammatory cells infiltration into the synovium, and diminished the erosive damage in the cartilage. CONCLUSION:The murine model with chronic hyperuricemia and gout be built in present study is consistent with the clinical symptoms of patients with long-standing hyperuricemia and acute gouty arthritis. RSG water extract has potent efficacy in ameliorating murine hyperuricemia and gout induced by PO and MSU.
Astilbin reduces ROS accumulation and VEGF expression through Nrf2 in psoriasis-like skin disease.
Wang Wuyuntana,Yuhai ,Wang Huan,Chasuna ,Bagenna
BACKGROUND:Psoriasis is a common and intractable skin disease affecting the physical and mental health of patients. The accumulation of ROS is involved in the pathogenesis of psoriasis and antioxidants are believed to be therapeutic. This study aimed to investigate the therapeutic efficacy of astilbin on ROS accumulation in psoriasis. RESULTS:The study showed that 50 μg/ml astilbin could inhibit the growth and reduce the accumulation of ROS in HaCaT cells stimulated by IL-17 and TNF-α. Astilbin could elevate the Nrf2 accumulation in the nuclei, eventually leading to the transcriptional activation of various antioxidant proteins and reducing the expression of VEGF. CONCLUSIONS:Our results collectively suggest that astilbin could induce Nrf2 nucleus translocation, which is contribute to reduce the ROS accumulation and VEGF expression, and inhibit the proliferation of HaCaT cells.
Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL-induced osteoclastogenesis.
Jin Haiming,Wang Qingqing,Chen Kai,Xu Ke,Pan Hao,Chu Feifan,Ye Zhen,Wang Ziyi,Tickner Jennifer,Qiu Heng,Wang Chao,Kenny Jacob,Xu Huazi,Wang Te,Xu Jiake
Journal of cellular and molecular medicine
Osteoporosis is the most common osteolytic disease characterized by excessive osteoclast formation and resultant bone loss, which afflicts millions of patients around the world. Astilbin, a traditional herb, is known to have anti-inflammatory, antioxidant and antihepatic properties, but its role in osteoporosis treatment has not yet been confirmed. In our study, astilbin was found to have an inhibitory effect on the RANKL-induced formation and function of OCs in a dose-dependent manner without cytotoxicity. These effects were attributed to its ability to suppress the activity of two transcription factors (NFATc1 and c-Fos) indispensable for osteoclast formation, followed by inhibition of the expression of bone resorption-related genes and proteins (Acp5/TRAcP, CTSK, V-ATPase-d2 and integrin β3). Furthermore, we examined the underlying mechanisms and found that astilbin repressed osteoclastogenesis by blocking Ca oscillations and the NF-κB and MAPK pathways. In addition, the therapeutic effect of MA on preventing bone loss in vivo was further confirmed in an ovariectomized mouse model. Therefore, considering its ability to inhibit RANKL-mediated osteoclastogenesis and the underlying mechanisms, astilbin might be a potential candidate for treating osteolytic bone diseases.
The flavonoid-enriched extract from the root of Smilax china L. inhibits inflammatory responses via the TLR-4-mediated signaling pathway.
Feng Haixing,He Yanling,La Lei,Hou Chuqi,Song Luyao,Yang Qin,Wu Fuling,Liu Wenqin,Hou Lianbing,Li Yan,Wang Chunxia,Li Yuhao
Journal of ethnopharmacology
ETHNOPHARMACOLOGICAL RELEVANCE:Smilax china L. has been used clinically to treat various inflammatory disorders with a long history. AIM OF THE STUDY:To investigate the mechanisms underlying anti-inflammatory action of the extract from the herb. MATERIALS AND METHODS:The extract was identified and quantified using the Ultra Performance Liquid Chromatography-Photo Diode Array-Mass Spectrometer method. The anti-inflammatory activities were examined in xylene-induced mouse ear edema and cotton ball-induced rat granuloma. The inflammatory mediators, pro-inflammatory cytokines and TLR-4-mediated signals in LPS-stimulated RAW264.7 macrophages were determined using ELISA, real-time PCR, Western blot and/or immunofluorescence, respectively. RESULTS:The extract was found to enrich flavonoids (44.3%, mainly astilbin, engeletin, isoastilbin, cinchonain Ia, quercetin-3-O-a-L-rhamnopyranoside and chlorogenic acid). The flavonoid-enriched extract (FEE) inhibited xylene-induced mouse ear edema and cotton ball-induced rat granuloma, and suppressed LPS-induced over-release and/or overexpression of tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide synthase, interleukin-1β and interleukin-6 in RAW264.7 macrophages. Mechanistically, FEE suppressed protein overexpression of TLR-4 and its downstream signals, MyD88 protein, phosphorylated inhibitory κB-α, NF-κB-P65 and MAPK p38, as well as phosphorylation of phosphoinositide 3-kinase (PI3K) p85α at Tyr and Akt at Ser in LPS-stimulated macrophages. The mode of the anti-inflammatory action of FEE was similar to that of TAK-242 (a selective TLR-4 inhibitor). CONCLUSIONS:The present results demonstrate that FEE inhibit inflammatory responses via the TLR-4-mediated signaling pathway. Our findings go a new insight into the mechanisms underlying anti-inflammatory action of the herb, and provide a better understanding of its use for inflammatory diseases.
Astilbin promotes the induction of regulatory NK1.1 CD4 NKG2D T cells through the PI3K, STAT3, and MAPK signaling pathways.
Han Sen,Lin Zhijie,Wen Jianqiang,Wu Keyan,Xu Yemin,Zhang Yu,Lu Guotao,Xiao Weiming,Ding Yanbing,Jia Xiaoqin,Deng Bin,Gong Weijuan
Astilbin is a potential agent for autoimmune and inflammatory diseases and has a protective effect in mice with DSS-induced colitis. NK1.1 CD4 NKG2D T cells are a subpopulation of regulatory T cells that produce TGF-β1 and IL-10. Whether astilbin directly promotes the induction of NK1.1 CD4 NKG2D T cells and whether these astilbin-stimulated T cells exert an immune-regulatory role remain unclear. Here, we show that astilbin efficiently induces the production of NK1.1 CD4 NKG2D T cells with high expressions of TGF-β1, IL-10, CCR6, and CCR9 in a dose-dependent manner ex vivo. These regulatory T cells also substantially inhibit the activities of CD8 T cells and macrophages. Intraperitoneal injection of astilbin ameliorates the severity of colitis with an increase in the frequency of NK1.1 CD4 NKG2D T cells in the colon tissue of DSS-treated mice. Moreover, adoptive transfer of NK1.1 CD4 NKG2D T cells induced by astilbin remarkably protects against the onset of DSS-induced colitis. Finally, the PI3K, STAT3, and MAPK signaling pathways are involved in the induction of NK1.1 CD4 NKG2D T cells by astilbin. Taken together, our study elucidates a new immune-regulatory mechanism of astilbin by inducing the regulatory NK1.1 CD4 NKG2D T cells and indicates a potential clinical use of astilbin for patients with inflammatory bowel diseases.
Astilbin protects against cerebral ischaemia/reperfusion injury by inhibiting cellular apoptosis and ROS-NLRP3 inflammasome axis activation.
Li Yu,Wang Rong,Xue Lian,Yang Yilin,Zhi Feng
BACKGROUND:Ischaemic stroke is a lethal cerebrovascular disease that occurs worldwide. Astilbin is a natural flavonoid compound with various physiological activities. The purpose of this study was to investigate the neuroprotective effects of Astilbin after cerebral ischaemia reperfusion (I/R) injury. METHODS:The oxygen and glucose deprivation (OGD) model was used to simulate cerebral I/R injury in vitro. Cell viability was measured via CCK-8 and LDH release assays. Cell apoptosis was measured via Hoechst 33258 staining and flow cytometry assays. ROS was detected via flow cytometry assay. The protein expression levels were determined by western blotting. The middle cerebral artery occlusion (MCAO) model was used to simulate cerebral I/R injury in vivo. Cerebral ischaemic volume was measured by TTC staining. The Zea-Longa score, rota-rod test, and foot-fault test were used to evaluate behavioural changes and neurological deficits in rats. RESULTS:Astilbin significantly enhanced cell viability and decreased LDH release after OGD treatment in vitro. Astilbin effectively curbed cell apoptosis induced by OGD via inhibiting the activation of caspase-3, decreasing the ratio of Bax/Bcl-2 and decreasing FADD. Astilbin also inhibited OGD-induced inflammation by suppressing ROS-NLRP3 inflammasome axis activation. Further results revealed that Astilbin could suppress the MAPK pathway and activate the PI3K/AKT pathway. Finally, Astilbin significantly reduced the cerebral infarction volume and relieved neurological deficits in rats in vivo. CONCLUSION:Astilbin could defend against cerebral I/R injury by inhibiting apoptosis and inflammation via suppressing the MAPK pathway and activating the AKT pathway.
Study on Anti-Inflammatory Effect and Major Anti-Inflammatory Components of PSORI-CM02 by Zebrafish Model.
Yuan Xiaohong,Huang Leyu,Lei Jiaqi,Long Yingxin,Li Cong
Evidence-based complementary and alternative medicine : eCAM
PSORI-CM02 is an optimization formula of PSORI-CM01, which is a clinical herbal formula for the treatment for psoriasis in the Guangdong Provincial Hospital of Chinese Medicine. Previous research indicates that it plays a critical role in anti-inflammation and immunoregulation. Rhizoma smilacis glabrae (RSG) is one herbal medicine of PSORI-CM02, whose effective anti-inflammatory component is astilbin. This study aims to test the anti-inflammatory and immunoregulation effects of astilbin as well as RSG in PSORI-CM02, and we, respectively, used the CuSO-induced neutrophil-specific transgenic zebrafish model and the melanin allele mutated Albino strain zebrafish model to visualize the effects of neutrophil recruitment and macrophage phagocytosis. Our data indicated that both PSORI-CM02 and astilbin had anti-inflammatory effects, leading to a reduction in the recruitment of neutrophils and promotion in macrophage phagocytosis. Nevertheless, the negative liquor of Rhizoma smilacis glabrae (PSORI-CM02 without RSG) also had anti-inflammatory and promoting macrophage phagocytosis effects. The results revealed the formula excluding RSG also had anti-inflammatory and immunoregulation effects, which demonstrated that RSG was not the major anti-inflammatory herbal medicine in PSORI-CM02. Similarly, astilbin was not the major anti-inflammatory active ingredient in the formula. The anti-inflammatory and the promotion of macrophage phagocytosis effect of PSORI-CM02 zebrafish were the results of multiple component interaction, which was the common characteristic of the Chinese medicine compound.
Astilbin influences the progression of osteoarthritis in rats by down-regulation of PGE-2 expression via the NF-κB pathway.
Yang Mao,Chen Chunlin,Wang Kun,Chen Yujiang,Xia Jingfu
Annals of translational medicine
Background:Osteoarthritis (OA) is the most common joint disease, affecting most middle-aged and elderly people. Astilin (AST) is the main active ingredient isolated from the traditional Chinese medicine Astilbe chinensis and has anti-inflammatory and anti-arthritis effects. The purpose of this study was to investigate the effect and mechanism of AST on OA in rats mediated by papain. Methods:In this study, in vivo experiments were conducted to investigate the protective effect and potential mechanism of Astilbin (AST) when it inhibited the development of osteoarthritis (OA). Results:A rat model of OA is constructed. Through HE staining, it is found that AST can protect the articular surface and reduce damage. The results of immunohistochemical staining also prove that AST can inhibit the expression of prostaglandin E2 (PGE2) and has an excellent inhibitory effect on inflammatory factors. It is found that AST can significantly inhibit the protein expression of interleukin 1 beta (IL-1β), TNF-α, and NF-κB. Polymerase Chain Reaction (PCR) assay shows that the mRNA of IL-1β, TNF-α, and NF-κB is down-regulated, which also proves that the protective mechanism of AST is related to the NF-κB pathway. Conclusions:In general, this study proves that AST can be a potential therapy for degenerative joint diseases, including OA.
Astilbin lowers the effective caffeine dose for decreasing lipid accumulation via activating AMPK in high-fat diet-induced obese mice.
Yang Licong,Zhu Yanping,Zhong Shusheng,Zheng Guodong
Journal of the science of food and agriculture
BACKGROUND:Caffeine has an anti-obesity effect, although chronic excessive caffeine consumption also causes caffeinism, which is marked by increased anxiety or depression, amongst other symptoms. The present study aimed to investigate whether the addition of flavonoids such as astilbin can reduce the caffeine dose needed to inhibit obesity. RESULTS:ICR mice (n = 80) were fed with normal diet, high-fat diet (HFD), HFD supplemented with astilbin, caffeine, or astilbin + caffeine for 12 weeks. When diets supplemented with astilbin, 0.3 g kg diet caffeine had the same effect as 0.6 g kg diet caffeine alone, and 0.6 g kg diet caffeine combined with astilbin most effectively inhibited HFD-induced obesity. Astilbin improved the anti-obesity effects of caffeine on lipid accumulation via the activation of AMP-activated protein kinase α (AMPKα). (i) Activated AMPKα decreased lipid biosynthesis by suppressing the activity or mRNA expression of 3-hydroxy-3-methylglutaryl-CoA reductase, sterol regulatory element binding protein 1c and its target gene fatty acid synthase. (ii) Activated AMPKα also up-regulated lipolysis by enhancing the expression of adipose triglyceride lipase and increasing the phosphorylation of hormone-sensitive lipase. (iii) Finally, activated AMPKα increased carnitine acyltransferase and acyl-CoA oxidase activities, which further promoted fatty acid β-oxidation. CONCLUSION:The results obtained in the present study indicate that astilbin may decrease the effective dose of caffeine needed for an anti-obesity effect and also suggest that it suppresses fat accumulation via the activation of AMPK. © 2020 Society of Chemical Industry.
Astilbin combined with lipopolysaccharide induces IL-10-producing regulatory B cells via the STAT3 signalling pathway.
Xu Yemin,Wu Keyan,Han Sen,Ding Shizhen,Lu Guotao,Lin Zhijie,Zhang Yu,Xiao Weiming,Gong Weijuan,Ding Yanbing,Deng Bin
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
OBJECTIVES:Astilbin exerts immunoregulatory activities and plays anti-inflammatory effects in inflammation-associated diseases. IL-10-producing B cells are the major subset of regulatory B cells (Bregs) and inhibit inflammation and autoimmune diseases. This study aimed to analyse the inducing effect of astilbin on Bregs and investigate the involved molecular mechanisms. METHODS:The frequencies and activities of IL-10-producing Bregs were observed using the co-treatment of astilbin and lipopolysaccharide (LPS) ex vivo. The protective effect of astilbin/LPS-induced Bregs on dextran sulphate sodium (DSS)-induced colitis was confirmed in vivo. The molecular signalling events of Breg induction were checked via Western blot. CD40 and toll-like receptor (TLR) 4 B cells were treated with astilbin/LPS to determine the modulatory role of CD40 or TLR4 on astilbin/LPS-induced Bregs. RESULTS:Although astilbin alone could not affect Bregs, the co-treatment of astilbin and LPS remarkably induced CD19 CD1d and CD19 TIM-1 cells which produced IL-10 ex vivo. Colonic CD19 CD1d and CD19 TIM-1 cells were also increased in astilbin-treated mice with DSS-induced colitis. The adoptive transfer of CD19 TIM-1 cells pre-induced by astilbin/LPS directly suppressed the progression of DSS-induced colitis. Combined astilbin and LPS stimulated the STAT3 activation of CD19 TIM-1 cells but had no effects on SOCS3, AKT, NF-κB, Erk, JNK nor P38. Inhibiting the STAT3 phosphorylation of CD19 TIM-1 cells abolished Breg induction by astilbin/LPS. Furthermore, Breg induction was weakened in CD40 B cells with the decrease in STAT3 activation, but had disappeared in TLR4 B cells with no STAT3 activation, thereby confirming the indispensable role of TLR4 signalling in the induction of IL-10-producing Bregs. CONCLUSIONS:This study reports the new immunoregulatory role of astilbin for promoting IL-10-producing B cells and suggests the possible use of astilbin in the therapy of inflammatory diseases.
Astilbin prevents osteoarthritis development through the TLR4/MD-2 pathway.
Sun Shuaibo,Yan Zijian,Shui Xiaolong,Qi Weihui,Chen Yanlin,Xu Xinxian,Hu Yuezheng,Guo Weijun,Shang Ping
Journal of cellular and molecular medicine
Osteoarthritis has become one of the main diseases affecting the life of many elderly people with high incidence of disability, and local chronic inflammation in the joint cavity is the most crucial pathological feature of osteoarthritis. Astilbin is the main active component in a variety of natural plants such as Hypericum perforatum and Sarcandra glabra, which possess antioxidant and anti-inflammatory effects. At present, there is no study about the protective effect of Astilbin for osteoarthritis. The purpose of this study was to investigate the effect of Astilbin in human OA chondrocytes and mouse OA model, which was established by surgery-mediated destabilization of the medial meniscus (DMM). In vitro, we found that Astilbin pre-treatment inhibited lipopolysaccharide (LPS)-induced overproduction of inflammation-correlated cytokines such as nitric oxide (NO), prostaglandin E2 (PGE2), tumour necrosis factor α (TNF-α) and interleukin 6 (IL-6), and suppressed overexpression of inflammatory enzymes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2). Astilbin, on the other hand, prevented the LPS-induced degradation of extracellular matrix (ECM) by down-regulating MMP13 (matrix metalloproteinases 13) and ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin motifs 5). Moreover, by inhibiting the formation of the TLR4/MD-2/LPS complex, Astilbin blocked LPS-induced activation of TLR4/NF-κB signalling cascade. In vivo, Astilbin showed the chondro-protective effect in the surgical-induced OA mouse models. In conclusion, our findings provided evidence that develops Astilbin as a potential therapeutic drug for OA patients.
Astilbin-induced inhibition of the PI3K/AKT signaling pathway decelerates the progression of osteoarthritis.
Chen Chunlin,Yang Mao,Chen Yujiang,Wang Yaoyao,Wang Kun,Li Tengxian,Hu Qing,Zhang Wenjing,Xia Jingfu
Experimental and therapeutic medicine
Degeneration and destruction of articular cartilage are the key characteristics of osteoarthritis (OA). In recent studies, the use of astilbin (AST), the primary active ingredient of , has been shown to correlate with a reduction in inflammatory disease symptoms. The present study aimed to investigate the effects and mechanisms of AST on OA. A rat model of OA was constructed and experiments were performed using the AST, PBS, OA and control groups. The cartilage tissues of each group were assessed by hematoxylin and eosin and toluidine blue staining. The gene expression levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, AKT, PI3K and other related proteins were analyzed by reverse transcription-quantitative PCR and western blot analysis. AST was found to significantly inhibit IL-1β and TNF-α protein expression; this further confirmed that IL-1β, TNF-α and PI3K mRNA expression was downregulated, indicating that the protective mechanism of AST is associated with the PI3K/AKT pathway. Overall, the results of the present study demonstrate that AST can improve OA symptoms by downregulating the PI3K/AKT signaling pathway, and may therefore be a potential therapeutic option for patients with OA.