Fluorescence intensity (λ_em = 483 nm) of compound 1-Cu²⁺ to various amino acids: the first bars represent the fluorescence intensity upon addition of 4 equivalents of various amino acids; the second bars represent the fluorescence intensity after subsequent addition of 2 equivalents of GSH to the non-sulfhydryl amino acids solution, respectively.

<p>Fluorescence intensity (λ_em = 483 nm) of compound 1-Cu²⁺ to various amino acids: the first bars represent the fluorescence intensity upon addition of 4 equivalents of various amino acids; the second bars represent the fluorescence intensity after subsequent addition of 2 equivalents of GSH to the non-sulfhydryl amino acids solution, respectively.</p

Synthesis procedures of the thiols probe (compound 1-Cu²⁺).

<p>Synthesis procedures of the thiols probe (compound 1-Cu²⁺).</p

Fluorescence responses of compound 1-Cu²⁺ (10 μmol/L) in CH₃CN:H₂O (3:2, v/v) PBS solution upon the addition of increasing GSH.

Insert: fluorescence titration profile at 483 nm upon the addition of GSH (excited at 445 nm).</p

UV-vis titration of compound 1 (10 μmol/L) in CH₃CN:H₂O (3:2, v/v) PBS solution upon addition of Cu²⁺.

<p>Inset: UV-vis titration profile of compounds <b>1</b> upon addition of Cu²⁺, the absorption was recorded at 480 nm.</p

Fluorescence emission spectra of compound 1 (10 μmol/L) in CH₃CN:H₂O (3:2, v/v) PBS solution with successive addition of Cu²⁺.

<p>Insert: fluorescence titration profile at 483 nm upon the addition of Cu²⁺ (excited at 445 nm).</p

DataSheet1_Dapagliflozin Protects Methamphetamine-Induced Cardiomyopathy by Alleviating Mitochondrial Damage and Reducing Cardiac Function Decline in a Mouse Model.ZIP

Background: Methamphetamine (METH)-induced cardiovascular toxicity has been attributed to its destructive effect on mitochondrial function at least to some extent. Previous studies highlighted the benefits of dapagliflozin (DAPA) on the cardiovascular system, but the response of METH-induced cardiomyopathy to DAPA is never addressed before. The present study aimed to investigate the potential ability of DAPA in preventing METH-induced cardiomyopathy.Materials and Methods: C57BL/6 mice were randomly divided into control group (n = 24), METH group (n = 24), and METH + DAPA group (n = 24). The METH-induced cardiomyopathy group received intraperitoneal METH injections at gradually increasing doses thrice weekly for 14 weeks. Mice in the METH + DAPA group were simultaneously treated with DAPA 1 mg/kg/day by intragastric administration. Echocardiography was performed to assess cardiac function. Reactive oxygen species (ROS), JC-1, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays were performed to evaluate oxidative stress, mitochondrial damage, and apoptosis, respectively. Mitochondrial and apoptosis-related protein expression was measured by western blotting.Results: Mice exposed to METH exhibited reduced cardiac function (left ventricular ejection fraction [LVEF]: 56.51 ± 6.49 vs. 73.62 ± 1.42, p Conclusion: DAPA protects against METH-induced cardiomyopathy in mice by decreasing mitochondrial damage and apoptosis.</p