Cryptotanshinone, a lipophilic compound of Salvia miltiorrriza root, inhibits TNF-α-induced expression of adhesion molecules in HUVEC and attenuates rat myocardial ischemia/reperfusion injury in vivo

Jin, Yong; Kim, Chun Wook; Kim, Young Min; Nizamutdinova, Irina Tsoy; Ha, Yu Mi; Kim, Hye Jung; Seo, Han Geuk; Son, Kun Ho; Jeon, Su Jin; Kang, Sam Sik; Kim, Yeong Shik; Kam, Sung Chul; Lee, Jea Heun; Chang, Ki Churl

doi:10.1016/j.ejphar.2009.04.038

Cited by 80 publications

(70 citation statements)

References 17 publications

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“…According to one recent report, salvia miltiorrhiza had showed the potential to treat severe acute pancreatitis by reducing the serum levels of IL-6, IL-8, and TNF-a [25]. One component of salvia miltiorrrhiza root is ''cryptotanshinone'' a lipophilic compound that inhibits NF-kB translocation, expression of pro-inflammatory cytokines (TNF-a, IL-1b, IL-6), neutrophil infiltration and MPO activity in ischemic myocardial tissues as well as significantly reduced plasma levels of TNF-a and IL-1b [26]. A second component of SK0506, ''gardenia jasminoides'', attenuates acute pancreatitis as well as pancreatitis-associated lung injury in mice as reflected by reductions in pancreatic edema, neutrophil infiltration, serum amylase, lipase, serum cytokine levels and mRNA expression of multiple inflammatory mediators [27].…”

Section: Discussionmentioning

confidence: 99%

Targeting BuChE-inflammatory Pathway by SK0506 to Manage Type 2 Diabetes and Alzheimer Disease

et al. 2009

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Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) affect a large percent of the population worldwide. Experimental studies have revealed that T2DM and AD share several molecular processes that underlie their respective degenerative pathology. Based on this information, we quantified TNF-α, IL-6 levels, serum glucose, serum triglyceride, hepatic triglyceride, serum AST, serum ALT and butyrylcholinesterase (BuChE) in various rat tissues. HFD was fed to rats resulting in increased body weight, fasting blood glucose, IL-6, TNF-α levels, hepatic triglyceride, serum AST, serum ALT and BuChE. SK0506 treatment significantly prevented weight gain induced by HFD feeding. SK0506, but not Rosiglitazone, significantly reduced serum and hepatic triglycerides levels. Treatment with SK0506 also ameliorated elevated levels of both inflammatory markers (TNF-α and IL-6) and serum liver enzymes (ALT and AST) significantly in HFD fed rats. BuChE activity also reduced in skeletal muscle and adipose tissues of rats treated by SK0506. In conclusion, current study has opened new potential avenues towards research for management of T2DM and AD by Chinese herbal extracts, ‘‘SK0506’’.

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Section: Discussionmentioning

confidence: 99%

Targeting BuChE-inflammatory Pathway by SK0506 to Manage Type 2 Diabetes and Alzheimer Disease

et al. 2009

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“…In 2009, Jin et al reported that CT reduces myocardial I/R injury by inhibiting tumor necrosis factor (TNF)-alpha-induced expression of adhesion molecules in rats. 9) Then, Park et al demonstrated that CT exerted neuroprotective effects in experimentally induced transient cerebral ischemic damage animals. 12) CT has also been reported to protect against myocadial hypoxia-induced mitochondrial apoptosis in vitro.…”

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confidence: 99%

“…7,8) Cryptotanshinone (CT) (Fig. 1), one of active ingredients of Salvia miltiorrhiza root, has been widely used in the treatment of cardiovascular diseases, 9) hematological abnormalities, 10) and hyperlipidemia. 11) Recently, the effects of CT on I/R injury have also been demonstrated by scientists.…”

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confidence: 99%

Cryptotanshinone Ameliorates Hepatic Normothermic Ischemia and Reperfusion Injury in Rats by Anti-mitochondrial Apoptosis

Sun

Yuan

et al. 2014

Biological & Pharmaceutical Bulletin

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Cryptotanshinone (CT), isolated from the dried roots of Salvia militorrhiza, has been reported to have protective effects on myocardial and cerebral ischemia/reperfusion (I/R) injury both in vitro and in vivo. However, its effects and underlying mechanism on hepatic I/R injury remain unclear. To investigate its effects on hepatic I/R injury, thirty male Sprague-Dawley rats were randomized into 3 groups: a sham group, a vehicle-treated hepatic I/R group and a CT-treated (50 mg/kg) group. The hepatic I/R and CT-treated groups were subjected to 60 min of normothermic ischemia of the left lateral lobe of the liver, followed by 4 h of reperfusion. The animals were then sacrificed to collect the serum and the left liver lobe for assay. Hepatic function was protected, as evidenced by significantly reduced alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA) levels in the CT-treated group as compared with I/R group. The terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) demonstrated significantly decreased apoptosis in the CT-administration animals. Western blotting demonstrated upregulation of the proapoptotic protein Bcl-2, as well as decreased levels of the activated form of caspase-3 and the cleaved form of its substrate, poly(ADP-ribose) polymerase (PARP) in the CT-treated group compared with those of the I/R group. In addition, the phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs) was inhibited by CT. Our data suggest that CT attenuates hepatic I/R injury by inhibiting the intrinsic pathway of apoptosis, mediated partly through the inhibition of JNK and p38 MAPK phosporylation.

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“…However, other mechanisms cannot be excluded. A previous study demonstrated that cryptotanshinone may inhibit proinflammatory cytokine production, reduce neutrophil infiltration and downregulate adhesion molecules through the inhibition of NF-κB-activation during ischemia and reperfusion and finally attenuate ischemia and reperfusion-induced microcirculatory disturbances (28). Therefore, anti-inflammatory action may also be involved in cryptotanshinone-induced cardiac protection.…”

Section: Discussionmentioning

confidence: 99%

Cryptotanshinone attenuates isoprenaline-induced cardiac fibrosis in mice associated with upregulation and activation of matrix metalloproteinase-2

Yang

Kui-ying

et al. 2012

Mol Med Report

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Abstract.Cryptotanshinone is an active ingredient of Salvia miltiorrhiza that has been used in traditional Chinese medicine for treating cardiovascular disorders. Thus, we investigated the effects of cryptotanshinone on cardiac fibrosis induced by isoprenaline and examined whether cardiac matrix metalloproteinase (MMP)-2 is involved in this process. Male C57BL/6 mice received a daily injection of 0.9% saline, 3 mg/kg isoprenaline or isoprenaline plus 20 mg/kg cryptotanshinone by gastric gavage for 2 weeks. In this study we demonstrated that cryptotanshinone was able to significantly ameliorate isoprenaline-induced cardiac fibrosis, which was associated with a marked upregulation and activation of MMP-2 in the ventricular myocardium. Additionally, we demonstrated that cryptotanshinone dose-dependently upregulated and activated MMP-2 in cultured cardiac fibroblasts. Moreover, incubation with cryptotanshinone also prevented the isoprenaline-induced downregulation and inactivation of MMP-2 in cultured cardiac fibroblasts. Taken together, our data suggest that cryptotanshinone is a novel and potent antifibrotic agent. The present findings further our understanding of the role of MMP-2 in cardiac fibrosis and the antifibrotic mechanisms of cryptotanshinone.

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Cryptotanshinone, a lipophilic compound of Salvia miltiorrriza root, inhibits TNF-α-induced expression of adhesion molecules in HUVEC and attenuates rat myocardial ischemia/reperfusion injury in vivo

Cited by 80 publications

References 17 publications

Targeting BuChE-inflammatory Pathway by SK0506 to Manage Type 2 Diabetes and Alzheimer Disease

Targeting BuChE-inflammatory Pathway by SK0506 to Manage Type 2 Diabetes and Alzheimer Disease

Cryptotanshinone Ameliorates Hepatic Normothermic Ischemia and Reperfusion Injury in Rats by Anti-mitochondrial Apoptosis

Cryptotanshinone attenuates isoprenaline-induced cardiac fibrosis in mice associated with upregulation and activation of matrix metalloproteinase-2

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