Tanshinone IIA inhibits the adipogenesis and inflammatory response in ox‐LDL‐challenged human monocyte‐derived macrophages via regulating miR‐130b/WNT5A

Limei, Yuan; Zhang, Zhiguo; Liu, Qingle; Wang, Xuechen; Fan, Li‐Hua

doi:10.1002/jcb.29375

Cited by 18 publications

(14 citation statements)

References 36 publications

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“…Tanshinone IIA, an active compound, has multiple pharmacological functions, such as anti-inflammation and antioxidation. After the exposure of Tanshinone IIA to atherosclerosis model which is established by THP-1-derived macrophages treated with ox-LDL, the expression of IL-1β, IL6, and TNF-α was decreased compared to the untreated group, and a further study revealed that Tanshinone IIA may decrease the inflammatory response by mediating miR-130b and WNT5A [47]. In this study, our results showed that CCL2 significantly upregulated the expression of IL-1β and IL-6 in hippocampi of rats, while the expression of IL-1β and IL-6 in hippocampi of rats pretreated with Tan IIA decreased.…”

Section: Discussionmentioning

confidence: 94%

Tanshinone IIA Alleviates CCL2-Induced Leaning memory and Cognition Impairment in Rats: A Potential Therapeutic Approach for HIV-Associated Neurocognitive Disorder

Liao

Chen

Long

et al. 2020

BioMed Research International

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Chemokine CC motif ligand 2 (CCL2) is one of the most recognized proinflammatory chemokines, and the expression of CCL2 in the cerebrospinal fluid of patients infected with HIV-1 is significantly higher than that of healthy people. As such, it is seen as an important cause of HIV-associated neurocognitive disorder (HAND). Our previous investigation has confirmed the pathological role of CCL2 in mediating brain damage leading to cognitive dysfunction. Currently, however, research on therapeutic drugs for the central nervous system targeting CCL2 is very limited. Our present study used brain stereotactic technology to induce cognitive impairment in rats by injecting CCL2 (5 ng) into the bilateral hippocampus. To investigate the protective effect and mechanism of Tanshinone IIA (25, 50, 75 mg/kg/d) on CCL2-induced learning memory and cognitive impairment in rats, we performed the Morris water maze (MWM) and novel object recognition tests (NORT) on the rats. The results showed that Tanshinone IIA significantly alleviated CCL2-induced learning memory and cognitive dysfunction. Further studies on the hippocampal tissue of the rats revealed that Tanshinone IIA treatment significantly increased the activity of SOD and GSH-Px while the level of MDA decreased compared to the model group. Additionally, the relative expression of apoptosis-associated genes caspase-3, caspase-8, and caspase-9 and inflammation-associated genes IL-1β and IL-6 in Tanshinone IIA-treated rats was lower than that in model rats. Finally, we confirmed hippocampal neuron loss and apoptosis by Nissl staining and TdT-mediated dUTP Nick end labeling (TUNEL). Taken together, these data imply that Tanshinone IIA can ameliorate CCL2-induced learning memory and cognitive impairment by impacting oxidative stress, inflammation, and apoptosis. Tanshinone IIA may be a potential therapeutic agent for the treatment of HAND.

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Section: Discussionmentioning

confidence: 94%

Tanshinone IIA Alleviates CCL2-Induced Leaning memory and Cognition Impairment in Rats: A Potential Therapeutic Approach for HIV-Associated Neurocognitive Disorder

Liao

Chen

Long

et al. 2020

BioMed Research International

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“…It plays a leading role in the occurrence and development of systemic inflammation. In the early stage of sepsis, a large amount of TNF-α is mainly produced by macrophages and neutrophils, and it is the initiator in the cascade reaction process of inflammatory mediators (Mokotedi et al, 2019;Xue et al, 2019;Yuan et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Parecoxib ameliorates renal toxicity and injury in sepsis‐induced mouse model and LPS ‐induced HK ‐2 cells

Guo

Chen

et al. 2021

Drug Dev Res

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Parecoxib is a selective COX‐2‐specific inhibitor, which has been demonstrated to inhibit sepsis‐induced systemic inflammation, but its role in sepsis‐induced acute kidney injury has not been studied. This study was designed to investigate the effects of Parecoxib on sepsis‐induced acute kidney injury. In this study, the mice sepsis model was established using an internationally recognized cecal ligation and puncture (CLP). Hematoxylin–eosin staining was performed to examine kidney injury. Biochemical kit was used to detect the expression of BUN and Cre in serum, and ELISA was used to detect the expression of inflammatory factors in renal tissue. Tunel staining was used to detect tissue apoptosis. Furthermore, CCK‐8 assay was used to detect the cell viability of HK‐2 cells and RT‐qPCR was used to detect the expression of LPS‐induced inflammatory factors in HK‐2 cells.TUNEL staining was used to detect the level of cell apoptosis. Finally, the expressions of COX‐2, p‐NF‐kB P65, p‐IKKβ, NF‐kB P65, IKKβ, Kim1, NGAL, iNOS, VEGF, VEGFR2, CD31 and apoptosis‐related proteins in renal tissues and HK‐2 cells were detected by Western blot. We discovered that parecoxib could alleviate renal pathological changes, reduce renal function injury, and inhibit renal pathology to inhibit the release of inflammatory factors in renal tissue. Parecoxib inhibited sepsis induced microvascular damage and apoptosis in renal tissue. Parecoxib reduced the inflammation and apoptosis of renal tubular epithelial cells induced by LPS. Our data suggest that Parecoxib ameliorates sepsis‐induced kidney injury, and may have potential as a novel therapeutic method for treating sepsis‐induced kidney injury.

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“…Moreover, Tan had varied biological capabilities, such as anti-oxidation, anti-apoptosis, anti-in ammation, anti-cancer, improving microcirculation, and anti-myocardial ischemia [26]. Yet, the molecular system allows Tan connected with atheroprotection is inadequately identi ed [4].…”

Section: Discussionmentioning

confidence: 99%

“…Traditional Chinese medicine shows an imperative in uence on the medical treatment of people, which acts as athero-protectors [4]. Tanshinones are the main e cient elements of the Chinese medicinal herb Salvia miltiorrhiza, also known as Danshen, which has been extensively utilized in Asian nations to avert and manage malignant tumors, in ammatory diseases and CVD [5].…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Attenuates Inflammatory Responses by Downregulating MicroRNA-23b, Upregulating TRIB1 and Inactivation of the TLR4/NF-κB Signaling Pathway in THP-1 Macrophages

Ji¹,

Li²,

Liu³

et al. 2020

Preprint

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Background: Atherosclerosis is a kind of chronic cardiovascular disease, and Tanshinone IIA (Tan) is a naturally derived anti-inflammatory compound. In this study, we aim to explore the biological role of Tan and regulatory mechanism in atherosclerosis.Methods: Firstly, the model of atherosclerosis mice was constructed. The area of atherosclerosis, the level of blood lipid and the content of inflammatory factors were measured in mice treated with Tan. After that, the differentially expressed microRNAs (miRNAs) were obtained by microarray analysis of mice plasma. The effect of miR-23b on cell migration ability, adhesion ability and inflammatory factor level of macrophages treated with Tan. After that, we determined the target mRNA of miR-23b through the bioinformatics analysis and the dual luciferase reporter gene assay. THP-1 macrophages were treated with miR-23b mimic or si-TRIB1 to detect the activity of the TLR4/NF-κB signaling pathway via immunohistochemistry.Results: Tan injection significantly improved atherosclerosis inflammation in mice, especially in mice treated with 90 mg/kg dose. miR-23b was obtained by differential screening, which can significantly inhibit the drug effect of Tan, and aggravate the occurrence of atherosclerosis. miR-23b targeted TRIB1, the decrease of TRIB1 also inhibited the drug effect of Tan. The up regulation of miR-23b enhanced the activity of TLR4/NF-κB pathway, and TLR4/NF-κB pathway inhibited the drug effect of Tan on the inflammatory response.Conclusion: Overall, Tan could protect macrophage against inflammation via inactivating TLR4/NF-κB pathway by down-regulating miR-23b and upregulating TRIB1, providing a novel theoretical foundation for treatment of atherosclerosis.

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Tanshinone IIA inhibits the adipogenesis and inflammatory response in ox‐LDL‐challenged human monocyte‐derived macrophages via regulating miR‐130b/WNT5A

Cited by 18 publications

References 36 publications

Tanshinone IIA Alleviates CCL2-Induced Leaning memory and Cognition Impairment in Rats: A Potential Therapeutic Approach for HIV-Associated Neurocognitive Disorder

Tanshinone IIA Alleviates CCL2-Induced Leaning memory and Cognition Impairment in Rats: A Potential Therapeutic Approach for HIV-Associated Neurocognitive Disorder

Parecoxib ameliorates renal toxicity and injury in sepsis‐induced mouse model and LPS ‐induced HK ‐2 cells

Tanshinone IIA Attenuates Inflammatory Responses by Downregulating MicroRNA-23b, Upregulating TRIB1 and Inactivation of the TLR4/NF-κB Signaling Pathway in THP-1 Macrophages

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