Effects Of Hyp Research Articles

Dose-Dependent Effect of Hyperoside on the Physicochemical and Gel Properties of Porcine Myofibrillar Proteins at Different NaCl Concentrations under Oxidative Stress.

The effects of HYP (10, 50, and 250 μM/g protein) on the physicochemical and gel properties of myofibrillar proteins (MPs) at different NaCl concentrations under oxidative stress were explored. The incorporation of HYP significantly reduced carbonyl content and decreased the loss of free amine groups in a dose-dependent manner, regardless of NaCl concentration. In addition, HYP induced a dose-dependent decrement in total sulfhydryl content regardless of NaCl concentration, which might result from the formation of thiol-quinone adducts via Michael addition. The surface hydrophobicity was significantly increased with HYP addition. Nevertheless, compared with samples treated with 50 μM/g HYP, 250 μM/g HYP caused a significant decrease in surface hydrophobicity, which might be due to the increase in the extent of MPs unfolding and the concomitant aggregation of MPs by hydrophobic interaction. Furthermore, HYP also showed a dose-dependent increment in the water-holding capacity (WHC) and gel strength of MPs gels, which might be due to more orderly crosslinks via fibrous filaments at 0.2 M NaCl and more regular and lamellar structures with smaller and more homogeneous pores at 0.6 M NaCl. In summary, HYP reduced the oxidation-mediated changes of physicochemical characteristics, preventing the oxidative damage of MPs and reinforcing the ordered crosslinks of MPs-MPs and MPs-HYP during thermal gelation, ultimately resulting in a better gel quality. These results provide a theoretical support for the practical application of HYP as a natural antioxidant in gel-type meat products.

Photosensitizers against pathogens: Model membranes characterization with hypericin

Enveloped viruses, i.e., comprising a phospholipidic membrane encapsulating their genetic material, are pathogens responsible for many diseases, often severe (e.g., COVID-19 and AIDS). Since the viral envelope has a fundamental role in their infectivity, it may represent a promising target for broad-spectrum antivirals. We are proposing the use of photosensitizers (PS), molecules that, in the presence of absorbable light, react with O2 triggering the production of reactive oxygen species, very strong oxidants capable of damaging biological structures, such as membranes. A specific PS called hypericin (hyp) exhibits not only a useful fluorescence in the orange spectral range, but also a strong antiviral activity toward enveloped viruses. In a recent article, we demonstrated it to be virucidal against SARS-CoV-2 not only in the presence of light, in accordance with its photodynamic properties, but also in dark conditions, revealing a multimodal mechanism of action. To characterize further the effects of hyp on coronavirus envelopes, we used phase-separated supported lipid bilayers (SLBs), an excellent model system to simulate biological membranes. We studied their morphology with Atomic Force Microscopy (AFM) and discovered that a substantial rearrangement occurs in the presence of hyp and light, and also in the dark at higher hyp concentrations; the effect is primarily visible in the ordered phase, the lipid rafts. We aim to address if hyp changes the membrane's mechanical properties (e.g., stiffness and fluidity) using fluorescence techniques such as FCS and FLIM in correlation with AFM-Force Spectroscopy. Additionally, since lipid rafts and phosphatidylserine (a lipid on the envelope) are believed to play a crucial role in viral infection and immune escape of SARS-CoV-2, respectively, we investigate if hyp multimodal antiviral activity is also related to a preferential interaction with specific lipids, by means of correlative AFM-fluorescence microscopy.

The role and mechanism of hyperoside against myocardial infarction in mice by regulating autophagy via NLRP1 inflammation pathway

Ethnopharmacological relevanceThe genus Hypericum are widely distributed in China. Hypericum perforatum L. (genus Hypericum, family Hypericaceae) has a long history as a traditional Chinese medicine, which was traditionally used for the treatment of emotional distress, cardiothoracic depression, and acute mastitis. Hyperoside (Hyp) extracted from Hypericum perforatum L. has been affirmed to exert therapeutic effects on cardiovascular diseases, with widespread existence in plants of genus Hypericum. Hyp could also be extracted from Crataegus pinnatifida Bunge (genus Crataegus pinnatifida Bunge, family Rosaceae), another traditional Chinese medicine that traditionally prevented and treated heart disease in China. The cardioprotection and mechanism of Hyp comprise anti-inflammation, anti-fibrosis, activation of autophagy, and reversal of cardiac remodeling. Aim of the studyThis study aimed to explore the Hyp effect against MI and its underlying mechanism. Materials and methodsThe MI model was constructed in the KM mice via a ligating surgery of the left anterior descending (LAD) coronary artery. Subsequently, the mice were divided into following seven groups: Sham group, MI group, MI + Hyp 9 mg/kg group, MI + Hyp18 mg/kg group, MI + Hyp36 mg/kg group, MI + Fosinopril group, and MI + Hyp-36 mg/kg+3-MA group. Each group was treated with Hyp in different concentrations or positive medicine for two weeks except for the sham group. After two weeks, we examined the cardiac function, electrocardiogram (ECG), myocardial hypertrophy in the non-infarct area, collagen volume fraction (CVF), perivascular collagen area (PVCA) in the infarct area, and several serum cytokines. Autophagy and inflammation in cardiomyocytes were assessed via measuring autophagy-associated proteins and NLRP1 inflammasome pathway related proteins. ResultsHyp reversed LV remodeling and adverse ECG changes through reducing CVF and myocardial hypertrophy. Additionally, Hyp treatment could reduce inflammation levels in cardiomyocytes, compared with those in MI group. Moreover, NLRP1inflammation pathway was activated after MI. Up-regulation of autophagic flux suppressed NLRP1 inflammation pathway after Hyp treatment. However, co-treatment with 3-MA abrogated above effects of Hyp. ConclusionsHyp had obvious protective effect on heart injury in MI mice. Echocanrdiographic and histological measurements demonstrated that Hyp treatment improved cardiac function, and ameliorated myocardial hypertrophy and fibrinogen deposition after MI. The partial mechanism is that Hyp could up-regulate autophagy after MI. Furthermore, the promotion of autophagic flux would suppress NLRP1 inflammation pathway induced by MI.

Hyperoside Protects Against Pressure Overload-Induced Cardiac Remodeling via the AKT Signaling Pathway

Background/Aims: Cardiac hypertrophy is a major predisposing factor for heart failure and sudden cardiac death. Hyperoside (Hyp), a flavonoid isolated from Rhododendron ponticum L., is a primary component of Chinese traditional patent medicines. Numerous studies have shown that Hyp exerts marked anti-viral, anti-inflammatory, anti-oxidant, anti-cancer, anti-ischemic, and particularly cardio-protective effects. However, the effects of Hyp on cardiac hypertrophy have not been explored. The aims of this study were to determine whether Hyp could protect against cardiac remodeling and to clarify the potential molecular mechanisms. Methods: Neonatal rat cardiac myocytes were isolated and treated with different concentrations of Hyp, then cultured with angiotensin II for 48 h. Mice were subjected to either aortic banding or sham surgery (control group). One week after surgery, the mice were treated with Hyp (20 mg/kg/day) or vehicle by oral gavage for 7 weeks. Hypertrophy was evaluated by assessing morphological changes, echocardiographic parameters, histology, and biomarkers. Results: Hyp pretreatment suppressed angiotensin II-induced hypertrophy in cardiomyocytes. Hyp exerted no basal effects but attenuated cardiac hypertrophy and dysfunction, fibrosis, inflammation, and oxidative stress induced by pressure overload. Both in vivo and in vitro experiments demonstrated that the effect of Hyp on cardiac hypertrophy was mediated by blocking activation of the AKT signaling pathway. Conclusion: Hyp improves cardiac function and prevents the development of cardiac hypertrophy via AKT signaling. Our results suggest a protective effect of Hyp on pressure overload-induced cardiac remodeling. Taken together, Hyp may have a role in the pharmacological therapy of cardiac hypertrophy.

Brief Hyperthermia Does not Worsen Outcome after Striatal Hemorrhage in Rats

Hyperthermia accelerates and increases ischemic brain damage. Owing to overlapping mechanisms of injury, many assume that hyperthermia also worsens outcome after intracerebral hemorrhage (ICH). However, clinical data do not conclusively prove this, and there is only one animal study examining the impact of hyperthermia. In that study (MacLellan and Colbourne, 2005), several hyperthermia protocols were administered after collagenase-induced ICH in rats; none worsened injury. While the collagenase model is widely used, it differs in important ways from another common model - injecting autologous blood directly into the brain. Thus, we evaluated the impact of immediate hyperthermia (HYP, 39 °C for 3 hr) after a 100-µL infusion of blood into the striatum of rats. This treatment, which markedly increases ischemic damage, was compared to control rats kept normothermic (NOR, 37 °C). Three separate experiments were done to measure: 1) edema at 24 hr, 2) edema at 72 hr, and 3) behavioral impairment and lesion size out to 1 month post-ICH. The HYP treatment did not significantly affect edema at 24 hr, but surprisingly, it modestly reduced edema at 72 hr and partly improved behavioral outcome. However, there were no lasting effects of HYP on behavior (e.g., skilled reaching) or the volume of tissue lost (NOR: 14.0 mm(3) vs. HYP: 14.5 mm(3)). In summary, our findings do not support the common belief that hyperthermia worsens outcome after ICH. Additional research is needed to determine whether more severe or prolonged heating or fever and its cause (e.g., infection) affect morbidity and mortality after ICH.