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Abstract Hypochlorous acid (HClO), one of the most important reactive oxygen species (ROS), is a potent antimicrobial agent for the immune system against invasive bacteria and a wide range of pathogens. Therefore, it is critical to develop sensitive and selective methods for visualization of HClO in biological samples. In this work, a two-photon fluorescent probe HN2-TP) with long-wavelength emission (far-red: 630 nm) based on rhodamine analogue for bioimaging HClO was developed. Owing to a specific HClO induced cyclization reaction, the new probe shows large fluorescence enhancement (about 106-fold), good linear range with high sensitivity (detection limit: 40 nM), high selectivity and fast response when monitoring HClO in vitro. More importantly, by successfully imaging HClO in living cells and tissues, this kind of two-photon fluorescent probe with long-wavelength emission is expected for accurate sensing in complex biosystems, which could eliminate undesired autofluorescence and self-absorption. Graphical abstract A novel two-photon fluorescent probe with long-wavelength emission is developed for highly sensitive and selective monitoring HClO in living cells and tissues. fx1 Highlights • Hypochlorous acid (HClO) is a potent antimicrobial agent for the immune system. • A long-wavelength two-photon probe was developed for bioimaging HClO in vivo. • This two-photon probe may present new avenues for accurate sensing applications. [ABSTRACT FROM AUTHOR]

To maximize the phocatalytic activity, semiconductor-based catalysts need to be properly modified in various methods. Here, a feasible synergistic strategy is proposed for enhancing the photocatalytic property. We firstly combine 2D ZnInS 4 –S nanosheets with amorphous CoB nanoparticles to obtain hybrid catalysts with Schottky junction and S vacancy engineering, and indicate that the CoB/ZnInS 4 –S with the synergistic effect owns efficiently improved photocatalytic antibacterial performance. Based on systematic characterization technologies and theoretical calculations, it is concluded that the wonderful photocatalytic activity of CoB/ZnIn 2 S 4 –S results from enhanced light-harvesting ability, accelerated charge-carriers separation, high specific surface area and more active sites. Moreover, the upward band bending resulted from the difference in work function between two components causes the directional electrons flow from ZnIn 2 S 4 –S to CoB, inhibiting the electron backflow and stimulating more reactive oxygen species (ROS) formation. Meanwhile, S vacancy can capture electrons to boost charge-carriers separation. As a result, the optimal 2CoB/ZnIn 2 S 4 –S composite can thoroughly inactivate 6.18-log of E. coli under 100 min of visible light illumination. Furthermore, we explored the damage degree of cell membrane by various characterizations to prove the thorough death of E. coli. It is desired that this work can offer some inspiration to develop more progressive photocatalytic systems by multiple effects engineering. Combing the merits of 2D ZnIn 2 S 4 nanosheets and CoB nanoparticals, a novel photocatalyst with synergistic effect including Schottky junction and S vacancy engineering was fabricated via a simple electrostatic self-assembly method. Due to the difference in work functions between ZnIn 2 S 4 and CoB, the upward band bending results in the directional flow of the photo-generated electrons from ZnIn 2 S 4 –S to CoB, and inhibits the electrons backflow. Meanwhile, S vacancies can capture electrons to boost charge-carriers separation. The efficient charge-carriers separation stimulates the generation of more reactive oxygen species (ROS). Finally, ROS and photo-generated h+ act synergistically on the cell membrane of E. coli , leading to the irreversible death of these cells. [Display omitted] • CoB/ZIS-S photocatalyst with Schottky junction and vacancy engineering was successfully fabricated. • DFT calculation reveals the charge transfer mechanism of photocatalytic reaction. • The establishment of Schottky barrier in CB/ZIS-S can effectively inhibit the backflow of electrons. • CoB/ZIS-S displays excellent performance for photocatalytic E. coli inactivation. [ABSTRACT FROM AUTHOR]

The Tongmai Yangxin pill (TMYX) is derived from the Zhigancao decoction recorded in Shang han lun by Zhang Zhongjing during the Han dynasty. TMYX is used for the clinical treatment of chest pain, heartache, and qi-yin-deficiency coronary heart disease. Previous studies have confirmed that TMYX can improve vascular endothelial function in patients with coronary heart disease by upregulating nitric oxide activity and then regulating vascular tension. Whether TMYX can further improve myocardial NR by upregulating NO activity and then dilating blood vessels remains unclear. This study aimed to reveal whether TMYX can further improve myocardial NR by upregulating NO activity and then dilating blood vessels. The underlying cAMP/PKA and NO-cGMP signaling pathway-dependent mechanism is also explored. The left anterior descending coronary arteries of healthy adult male SD rats were ligated to establish the NR model. TMYX (4.0 g/kg) was orally administered throughout the experiment. Cardiac function was measured through echocardiography. Thioflavin S, Evans Blue, and TTC staining were used to evaluate the NR and ischemic areas. Pathological changes in the myocardium were assessed by hematoxylin–eosin staining. An automated biochemical analyzer and kit were used to detect the activities of myocardial enzymes and myocardial oxidants, including CK, CK-MB, LDH, reactive oxygen species, superoxide dismutase, malonaldehyde, and NO. The expression levels of genes and proteins related to the cAMP/PKA and NO/cGMP signaling pathways were detected via real-time fluorescence quantitative PCR and Western blot analysis, respectively. A microvascular tension sensor was used to detect coronary artery diastolic function in vitro. TMYX elevated the EF, FS, LVOT peak, LVPWd and LVPWs values, decreased the LVIDd, LVIDs, LV-mass, IVSd, and LV Vols values, demonstrating cardio-protective effects, and reduced the NR and ischemic areas. Pathological staining showed that TMYX could significantly reduce inflammatory cell number and interstitial edema. The activities of CK, LDH, and MDA were reduced, NO activity was increased, and oxidative stress was suppressed after treatment with TMYX. TMYX not only enhanced the expression of Gs-α, AC, PKA, and eNOS but also increased the expression of sGC and PKG. Furthermore, TMYX treatment significantly decreased ROCK expression. We further showed that TMYX (25–200 mg/mL) relaxed isolated coronary microvessels. TMYX attenuates myocardial NR after ischemia and reperfusion by activating the cAMP/PKA and NO/cGMP signaling pathways, further upregulating NO activity and relaxing coronary microvessels. Image 1 [ABSTRACT FROM AUTHOR]

Tongmai Yangxin pill (TMYX) is derived from the Zhigancao decoction recorded in Shang han lun by Zhang Zhongjing during the Han dynasty and was further improved by Professor Ruan Shiyi, a cardiovascular expert at Tianjin University of Traditional Chinese Medicine. TMYX is used for the clinical treatment of chest pain, heartache, and qi-yin-deficiency coronary heart disease and can improve vascular endothelial function in patients with angina pectoris or coronary heart disease by up-regulating nitric oxide activity and then regulating vascular tension. Whether TMYX can further improve myocardial no-reflow by up-regulating NO activity and then dilating blood vessels remains unclear. This study aimed to reveal whether TMYX can further improve myocardial NR by up-regulating NO activity and then dilating blood vessels. The mechanism underlying PI3K/Akt/eNOS pathway activation and apoptosis regulation is also explored. The left anterior descending coronary arteries of healthy adult male SD rats were ligated to establish a NR model. The rats were assigned to 14 groups: control, sham, NR, TMYX (4.0 g/kg), sodium nitroprusside (SNP), Tongxinluo capsule (TXL), PI3K blocker (LY), TMYX + LY, SNP + LY, TXL + LY, eNOS blocker (L-NAME), TMYX + L-NAME, SNP + L-NAME, and TXL + L-NAME groups. Cardiac function was measured through echocardiography. Thioflavin S, Evans Blue, and TTC staining were adopted to evaluate NR and ischemic areas. Cell inflammation degree and edema were assessed by hematoxylin–eosin staining. Automated biochemical analyzer and kit were used to detect the activities of myocardial oxidants, including reactive oxygen species, super oxide dismutase, malonaldehyde, and NO. The expression levels of genes and proteins in the PI3K/Akt/eNOS signaling pathway and apoptosis were detected via real-time fluorescence quantitative PCR and Western blot analysis, respectively. A microvascular tension sensor was adopted to detect coronary artery diastolic function in vitro. TMYX reduced NR and ischemic areas; suppressed LV-mass; enhanced EF, FS, LVOT peak, and LVSV; and improved cardiac structure and function. Moreover, it decreased creatine kinase (CK), CK-MB, and lactic dehydrogenase activities. TMYX increased NO and super oxide dismutase activities; inhibited malonaldehyde activity; reduced muscle fiber swelling and inflammatory cell infiltration; and improved vasodilation in vitro. In the NR myocardium, TMYX stimulated myocardial PI3K activities and PI3K (Tyr458) phosphorylation and enhanced Akt activities and Akt phosphorylation at Tyr315. TMYX increased the activities of eNOS and the phosphorylation of eNOS at Ser1177 in the NR myocardium and attenuated cardiomyocyte apoptosis by increasing the expression of Bcl-2 and decreasing that of caspase-3 and Bax. All these effects of TMYX were abolished by the specific inhibitors of PI3K (LY) and eNOS (L-NAME). TMYX attenuates myocardial NR after ischemia and reperfusion by activating the PI3K/Akt/eNOS pathway and regulating apoptosis, further up-regulating NO activity and relaxing coronary microvessels. Image 1 • TMYX improved the area of no-reflow and ischemia, and increased the content of NO, SOD activity and vasodilating function. • TMYX enhanced PI3K activities , stimulated Akt activities and increased eNOS activities. • TMYX increased the expression of Bcl-2, decreased Caspase-3 and Bax expression. • TMYX improved no-reflow by activating PI3K/Akt/eNOS pathway and regulating apoptosis. [ABSTRACT FROM AUTHOR]