RETRACTED: Tetramethylpyrazine alleviates lipopolysaccharide-induced damage in ATDC5 cells via down-regulating MyD88

Li, Qiang; Xing, Wen; Xiong, Xu; Wang, Sulong; He, Yao; Wang, Yueshu; Sun, Hongbin

doi:10.1016/j.yexmp.2019.104317

Cited by 5 publications

(10 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to synthetic substances, an increasing number of natural products and extracts of Traditional Chinese medicine (TCM) have also been proven to inhibit OA to varying degrees. [79][80][81][82][83][84] Due to the complex composition of TCM, there was no sufficient evidence supporting its role in delaying the process of OA in the past. However, the effects of TCM exacts have been fully demonstrated in relevant experiments that were carried out recently.…”

Section: P38mapk Pathway As Therapeutic Targets In Oa Treatmentmentioning

confidence: 99%

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

Dai

Yang

et al. 2022

JIR

View full text Add to dashboard Cite

Osteoarthritis (OA) is an aging-related joint disease, pathologically featured with degenerated articular cartilage and deformation of subchondral bone. OA has become the fourth major cause of disability in the world, imposing a huge economic burden. At present, the pathogenesis and pathophysiology of OA are still unclear. Complex regulating networks containing different biochemical signaling pathways are involved in OA pathogenesis and progression. The p38MAPK signaling pathway is a member of the MAPK signaling pathway family, which participates in the induction of cellular senescence, the differentiation of chondrocytes, the synthesis of matrix metalloproteinase (MMPs) and the production of pro-inflammatory factors. In recent years, studies on the regulating role of p38MAPK signaling pathway and the application of its inhibitors have attracted growing attention, with an increasing number of in vivo and in vitro studies. One interesting finding is that the inhibition of p38MAPK could suppress chondrocyte inflammation and ameliorate OA, indicating its therapeutic role in OA treatment. Based on this, we reviewed the mechanisms of p38MAPK signaling pathway in the pathogenesis of OA, hoping to provide new ideas for future research and OA treatment.

show abstract

Section: P38mapk Pathway As Therapeutic Targets In Oa Treatmentmentioning

confidence: 99%

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

Dai

Yang

et al. 2022

JIR

View full text Add to dashboard Cite

show abstract

“…Our findings firstly demonstrated the potential regulation mechanism between AS-IV and miR-203 in LPS-induced ATDC5 cell damage that miR-203 was up-regulated by AS-IV to alleviate inflammatory damage. Furthermore, MyD88 is a key downstream adaptor for most Toll-like regulators and IL-1 receptors, it takes key roles in elevating the signal transduction of downstream inflammatory factors (Li et al 2019;Qiao et al 2019). Li et al (2019) found that tetramethylpyrazine attenuated LPS-triggered ATDC5 cell injury through down-regulating MyD88.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, MyD88 is a key downstream adaptor for most Toll-like regulators and IL-1 receptors, it takes key roles in elevating the signal transduction of downstream inflammatory factors (Li et al 2019;Qiao et al 2019). Li et al (2019) found that tetramethylpyrazine attenuated LPS-triggered ATDC5 cell injury through down-regulating MyD88. Consistently, we also found that up-regulation of MyD88 enhanced LPS-induced inflammatory damage, while MyD88 knockdown inhibited this damage.…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV protects ATDC5 cells from lipopolysaccharide-caused damage through regulating miR-203/MyD88

Yang

et al. 2020

Pharmaceutical Biology

View full text Add to dashboard Cite

Context: Osteoarthritis (OA) is a degenerative arthrosis sickness. Astragaloside IV (AS-IV) functions by relieving inflammatory damage. Objective: We aimed to investigate the mechanism by which AS-IV protects ATD cells from lipopolysaccharide (LPS)-induced damage. Materials and methods: ATDC5 cells were transfected with miR-203 inhibitor and NC inhibitor (150 nM) or pEX-MyD88 and sh-MyD88 (50 nM) for 48 h, pre-treated by 15 lg/mL AS-IV for 24 h, then treated by 5 lg/mL LPS for 12 h. Dual-luciferase activity testing was used to determine whether miR-203 could bind to MyD88. CCK-8 and flow cytometry were used to detect cell activity and apoptosis, respectively, and qRT-PCR, western blots, and ELISA were performed to detect expression levels of miR-203 and inflammatory cytokines. Results: Based on the 50% inhibiting concentration (IC 50), there was no significant difference of AS-IV (0 to 15 lg/mL) on cell viability. Fifteen lg/mL was the optimal concentration of AS-IV in treating LPSinduced inflammatory damage in subsequent experiments since this was a semi-lethal concentration. AS-IV significantly reduces LPS-induced viability, apoptosis and the release of TNF-a, IL-6 and iNOS mainly through up-regulating miR-203. Further, MyD88 was a target gene of miR-203 and negatively regulated by miR-203. Knockdown of MyD88 inhibited LPS-induced inflammatory damage by inhibiting the NF-jB signal pathway. Discussion and conclusions: AS-IV protects ATDC5 cells against LPS-induced damage mainly via regulating miR-203/MyD88. Our results support a theoretical basis for in-depth study of the function of AS-IV and the clinical cure of OA.

show abstract

“…Clinically, the mortality of sepsis patients with delirium, shock and other symptoms is higher. In the past few years, observation methods have been used in most cell physiology studies (Andrikopoulos et al;Dal-Pizzol et al, 2014;Kuperberg and Wadgaonkar, 2017;Qiang et al, 2019). To better understand the occurrence, development and other pathological changes in the inflammatory reactions that occur in vivo during sepsis, clinically relevant animal models of sepsis or septic shock are needed (Andrikopoulos et al;Stare et al, 2015;Arslan et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the rats in the TMP group had diarrhea and other symptoms at the beginning. However, the symptoms were basically controlled within 1 hour after the injection of TMP (Qiang et al, 2019;Dong et al, 2019). These results demonstrate that TMP can significantly inhibit the secretion of inflammatory cytokines to block inflammatory reactions.…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine Ameliorates Lipopolysaccharide-Induced Sepsis in Rats via Protecting Blood–Brain Barrier, Impairing Inflammation and Nitrous Oxide Systems

Huang

Xie²,

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

The aim of this study was to assess the underlying impact of Tetramethylpyrazine (TMP), which is the main activity compound of Ligusticum chuanxiong Hort, on the blood–brain barrier, inflammatory and nitrous oxide systems in a rat model of lipopolysaccharide (LPS)-induced sepsis. The SD rats were divided into control group, LPS treatment group, and LPS + TMP treatment group. TMP administered by tail vein injection. The mortality of experimental rats was recorded during the experiment. Rats were sacrificed after 14 days. Peripheral blood was collected and the expression levels of inflammatory factors TNF-α, IL-1β, and IL-6 were detected by ELISA. The integrity of blood-brain barrier was detected by sodium fluorescein staining. Lung and brain tissues were taken to detect the infiltration of immune cells. Immunohistochemistry was performed to detect the expression of tight junctions related proteins and oxidative stress-related proteins. The results showed that TMP treatment for 14 days significantly decreased the weight loss and increased the survival rate of the septic rats significantly. TMP decreased the infiltration of inflammatory cells and alleviated the sepsis-induced damage in both the lung and brain tissues. The inflammatory cytokines TNF-α, IL-1β, and IL-6, were significantly decreased post-TMP treatment. Histopathological analysis with sodium fluorescein staining density showed that TMP had a protective effect on the basal lamina and cerebral cortex. Also, TMP significantly increased expression of the tight junction-related proteins claudin-5 and occludin in the brain tissue and increased the expression of the ZO-1 , Occludin , and Claudin-5 genes, indicating alleviated the degree of blood–brain barrier destruction. Furthermore, immunohistochemistry (IHC) and immunoblotting confirmed that TMP could inhibit the indicators of the nitrous oxide system, iNOS and eNOS; in addition, TMP significantly decreased the levels of MDA and NO. The findings showed that TMP treatment during sepsis was associated with the protection of the blood–brain barrier and the suppression of inflammatory reactions and the nitrous oxide system. This study reveals a promising protective role of TMP in septic encephalopathy and may suggest a therapeutic approach for fighting the deadly disease of sepsis in the clinic.

show abstract

RETRACTED: Tetramethylpyrazine alleviates lipopolysaccharide-induced damage in ATDC5 cells via down-regulating MyD88

Cited by 5 publications

References 32 publications

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

p38MAPK Signaling Pathway in Osteoarthritis: Pathological and Therapeutic Aspects

Astragaloside IV protects ATDC5 cells from lipopolysaccharide-caused damage through regulating miR-203/MyD88

Tetramethylpyrazine Ameliorates Lipopolysaccharide-Induced Sepsis in Rats via Protecting Blood–Brain Barrier, Impairing Inflammation and Nitrous Oxide Systems

Contact Info

Product

Resources

About