Atorvastatin affects the tissue concentration of hydrogen sulfide inmouse kidneys and other organs*

Wiliński, Bogdan; Wiliński, Jerzy; Somogyi, E; Piotrowska, Joanna; Góralska, Marta

doi:10.1016/s1734-1140(11)70414-5

Cited by 26 publications

(16 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Statins are shown to increase H 2 S level by inhibiting its metabolism [47]. Administration of SQR inhibitors can potentially inhibit H 2 S breakdown [48].…”

Section: Discussionmentioning

confidence: 99%

Exogenous Hydrogen Sulfide Attenuates High Glucose-Induced Cardiotoxicity by Inhibiting NLRP3 Inflammasome Activation by Suppressing TLR4/NF-κB Pathway in H9c2 Cells

Huang

Zhuang

Xie

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: This study aimed to investigate whether exogenous hydrogen sulfide (H₂S) confered cardiac protection against high glucose (HG)-induced injury by inhibiting NLRP3 inflammasome activation via a specific TLR4/NF-κB pathway. Methods: H9c2 cardiac cells were exposed to 33 mM glucose for 24 h to induce HG-induced cytotoxicity. The cells were pretreated with NaHS (a donor of H₂S) before exposure to HG. Cell viability, cell apoptosis, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and TLR4, NF-κB, NLRP3 inflammasome, IL-1β, IL-18 and caspase-3 expression were measured by standard methods. Results: H₂S attenuated HG-induced cell apoptosis, ROS expression and loss of MMP and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL-1β, IL-18 and caspase-3. In addition, H₂S inhibited the HG-induced activation of TLR4 and NF-κB. Furthermore, NLRP3 inflammasome activation was regulated by the TLR4 and NF-κB pathway. Conclusion: The present study demonstrated for the first time that H₂S appears to suppress HG-induced cardiomyocyte inflammation and apoptosis by inhibiting the TLR4/NF-κB pathway and its downstream NLRP3 inflammasome activation. Thus H₂S might possess potential in the treatment of diabetic cardiomyopathy.

show abstract

“…Statins are shown to increase H 2 S level by inhibiting its metabolism [47]. Administration of SQR inhibitors can potentially inhibit H 2 S breakdown [48].…”

Section: Discussionmentioning

confidence: 99%

Exogenous Hydrogen Sulfide Attenuates High Glucose-Induced Cardiotoxicity by Inhibiting NLRP3 Inflammasome Activation by Suppressing TLR4/NF-κB Pathway in H9c2 Cells

Huang

Zhuang

Xie

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Endogenous H 2 S in mammalian cells is known to be regulated by enzyme pathways such as cystathionine gamma lyase (CSE) and cystathionine beta synthase (CBS) . Statins, known as a class of cholesterol‐lowering drugs, could up‐regulate the CSE expression, and subsequently elevate the H 2 S generation in cells . Gu et al.…”

Section: Bodipy‐based Probes For Biothiolsmentioning

confidence: 99%

BODIPY‐Based Fluorescent Probes for Biothiols

Zhang

Wang

et al. 2020

Chemistry A European J

173

View full text Add to dashboard Cite

Fluorescent probes for biothiols have aroused increasing interest owing to their potential to enable better understanding of the diverse physiological and pathological processes related to the biothiol species. BODIPY fluorophores exhibit excellent optical properties, which can be readily tailored by introducing diverse functional units at various positions of the BODIPY core. In the present review, the development of fluorescent probes based on BODIPYs for the detection of biothiols are systematically summarized, with emphasis on the preferable detection of individual biothiols, as well as simultaneous discrimination among cysteine (Cys), homocysteine (Hcy), reduced glutathione (GSH). In addition, organelle‐targeting probes for biothiols are also highlighted. The general design principles, various recognition mechanisms, and biological applications are elaboratively discussed, which could provide a useful reference to researchers worldwide interested in this area.

show abstract

“…Clearly these are unrealistically high, however, they are nevertheless suggestive of drug perturbation of intracellular sulfide. Using the same methods, this group also observed that the statin, atorvastatin, substantially increased kidney H 2 S and slightly increased H 2 S in brain heart and liver [134]. Wójcicka et al [135] also observed that atorvastatin increased H 2 S production in perivascular adipose tissue by producing coenzyme Q 9 deficiency and thereby inhibiting mitochondrial oxidation.…”

Section: Other Questions Remaining and Future Directionsmentioning

confidence: 97%

Biology and therapeutic potential of hydrogen sulfide and hydrogen sulfide-releasing chimeras

Kashfi

Olson

2013

Biochemical Pharmacology

282

189

View full text Add to dashboard Cite

Hydrogen sulfide, H2S, is a colorless gas with a strong odor that until recently was only considered to be a toxic environmental pollutant with little or no physiological significance. However, the past few years have demonstrated its role in many biological systems and it is becoming increasingly clear that H2S is likely to join nitric oxide (NO) and carbon monoxide (CO) as a major player in mammalian biology. In this review, we have provided an overview of the chemistry and biology of H2S and have summarized the chemistry and biological activity of some natural and synthetic H2S-donating compounds. The naturally occurring compounds discussed include, garlic, sulforaphane, erucin, and iberin. The synthetic H2S donors reviewed include, GYY4137; cysteine analogs; S-propyl cysteine, S-allyl cysteine, S-propargyl cysteine, and N-acetyl cysteine. Dithiolethione and its NSAID and other chimeras such as, L-DOPA, sildenafil, aspirin, diclofenac, naproxen, ibuprofen, indomethacin, and mesalamine have also been reviewed in detail. The newly reported NOSH-aspirin that releases both NO and H2S has also been discussed.

show abstract

Atorvastatin affects the tissue concentration of hydrogen sulfide inmouse kidneys and other organs*

Cited by 26 publications

References 31 publications

Exogenous Hydrogen Sulfide Attenuates High Glucose-Induced Cardiotoxicity by Inhibiting NLRP3 Inflammasome Activation by Suppressing TLR4/NF-κB Pathway in H9c2 Cells

Exogenous Hydrogen Sulfide Attenuates High Glucose-Induced Cardiotoxicity by Inhibiting NLRP3 Inflammasome Activation by Suppressing TLR4/NF-κB Pathway in H9c2 Cells

BODIPY‐Based Fluorescent Probes for Biothiols

Biology and therapeutic potential of hydrogen sulfide and hydrogen sulfide-releasing chimeras

Contact Info

Product

Resources

About