Litsea cubeba essential oil: Extraction, chemical composition, antioxidant and antimicrobial properties, and applications in the food industry.

Litsea cubeba (Lour.) Pers. (Lauraceae) is a valuable industrial crop that produces essential oil. The essential oil extracted from L. cubeba (LCEO) has broad-spectrum antimicrobial activity and high antioxidant properties, with great potential for increased usage in the food industry. This literature review summarizes the extraction techniques, content and chemical composition, and antioxidant and antimicrobial activities of LCEO, with a focus on its usage in the food industry, which is an area of substantial recent research. The chemical composition of LCEO, which is affected by various factors, plays a key role in determining its bioactivity and usage in food. The potent antimicrobial activity of LCEO against various foodborne pathogens gives it potential for use in food packaging and preservation to extend shelf life. Future research challenges include the elucidation of the role and mechanism of individual chemical components of LCEO in inhibiting specific foodborne microorganisms; cultivar development to produce germplasm that yields essential oils of the desired chemical composition; and the development of commercial products that can be used in the food industry.

Multifunctional sprayable carboxymethyl chitosan/polyphenol hydrogel for wound healing.

The use of facile methods to synthesize environmentally friendly and multifunctional hydrogel dressings is still a major challenge in development. Herein, Turkish gall extract (TGE) and carboxymethyl chitosan (CMCS) were combined and sprayed using a dual syringe to form a multifunctional TGE-CMCS hydrogel (TC gel) in one step through abundant hydrogen bonding between functional groups as a green approach. TC gel showed rapid gelation at 19.0 ± 2.9 s. Apart from the advantage of being able to adapt to different wound shapes, TC gel retained the antioxidant, antibacterial, hemostatic and anti-inflammatory properties of TGE. In vitro antibacterial experiments showed that TC-gel eliminated 98.27 ± 0.79 % of Staphylococcus aureus and 98.87 ± 1.08 % of Escherichia coli. Compared with TGE or CMCS alone, TC gel accelerates skin wound healing due to its three-dimensional network structure and continuous release of active components at the wound site, enhancing re-epithelialization, improving collagen deposition, and increasing angiogenesis. The wound healing rate of full-thickness skin defect rats treated with TC gel was 93.98 ± 0.63 % on the 10th day. These results suggest that TC gel combined with a facile and scalable manufacturing method is a promising multifunctional wound dressing for clinical wound management.

Value of the virtual monoenergetic image from dual-layer dual-energy computed tomography enterography in the preoperative assessment of the internal penetrating complication of Crohn's disease.

BACKGROUND: To determine the utility of virtual-monoenergetic imaging (VMI) at low energy levels from contrast-enhanced dual-layer dual-energy (DLDE) computed tomography enterography (CTE) in the preoperative assessment of internal penetrating lesions of Crohn's disease (CD). MATERIALS AND METHODS: Thirty-eight patients with penetrating lesions of CD by surgery undergoing contrast-enhanced DLDE CTE were retrospectively included. Polyenergetic imaging (PEI) and VMIs at low energy levels [40-70 kiloelectron volts (keV)] with 10 keV intervals were reconstructed. The objective parameters of image quality [noise, signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR)] and the subjective parameter of image quality [diagnostic performance of lesions (DPL), overall image quality(OIQ)] of PEI and all VMIs at the low energy level were compared to determine the VMI on the optimal energy level. The lesion detection capability between PEI and the optimal VMI was compared. RESULTS: VMI40 was determined to be the optimal VMI among all VMIs at the low energy level for owning the best image quality. No significant difference was found in the detecting capability in penetrating lesions between VMI40 and PEI (p = 1.0), whereas a significant difference was found in the detecting capability in the bowel origin of the penetrating lesions (p = 0.004), the involved organ or structure by the fistula (p = 0.016) and the orifice of the fistula connected to the involved organ or structure ( p = 0.031) between them. CONCLUSIONS: Compared to conventional PEI, VMI40 improves the detection capability in anatomical details of penetrating lesions of CD, helping colorectal surgeons rationalizing preoperative plans of internal penetrating lesions of CD.

Effect of Low Dietary Folate on Mouse Spermatogenesis and Spindle Assembly Checkpoint Dysfunction May Contribute to Folate Deficiency-Induced Chromosomal Instability in Cultured Mouse Spermatogonia.

Folate, as the initial substrate in one-carbon metabolism, is involved in the synthesis of important substances such as DNA, RNA, and protein. Folate deficiency (FD) is associated with male subfertility and impaired spermatogenesis, yet the underlying mechanisms are poorly understood. In the present study, we established an animal model of FD to investigate the effect of FD on spermatogenesis. GC-1 spermatogonia were used as a model to investigate the effect of FD on proliferation, viability, and chromosomal instability (CIN). Furthermore, we explored the expression of core genes and proteins of spindle assembly checkpoint (SAC), a signaling cascade ensuring accurate chromosome segregation and preventing CIN during mitosis. Cells were maintained in medium containing 0, 20, 200, or 2000 nM folate for 14 days. CIN was measured by using a cytokinesis-blocked micronucleus cytome assay. We found that sperm counts decreased significantly (p < 0.001) and the rate of sperm with defects in the head increased significantly (p < 0.05) in FD diet mice. We also found, relative to the folate-sufficient conditions (2000 nM), cells cultured with 0, 20, or 200 nM folate exhibited delayed growth and increased apoptosis in an inverse dose-dependent manner. FD (0, 20, or 200 nM) significantly induced CIN (p < 0.001, p < 0.001, and p < 0.05, respectively). Moreover, FD significantly and inverse dose dependently increased the mRNA and protein expression of several key SAC-related genes. The results indicate that FD impairs SAC activity, which contributes to mitotic aberrations and CIN. These findings establish a novel association between FD and SAC dysfunction. Thus, FD-impaired spermatogenesis may be partly due to genomic instability and proliferation inhibition of spermatogonia.

Association of cataract extraction and the risk of dementia-A systematic review and meta-analysis.

Objectives: This research aims to investigate if cataract extraction lowers the risk of all-cause dementia. Methods: Original literature on cataract surgery associated with all-cause dementia as of November 27, 2022, was searched in several commonly used databases. Manual review was used to include eligible studies. Stata software (version 16) was used to perform statistical analysis on pertinent data. Publication bias can be precisely evaluated using funnel plots and Egger's test. Results: In the meta-analysis of 4 cohort studies with 245,299 participants. Pooled analysis indicated that cataract surgery was linked to a lower incidence of all-cause dementia (OR = 0.77, 95%CI: 0.66-0.89; I2= 54.7%; P < 0.001). Cataract surgery was linked to a lower risk of AD (OR = 0.60, 95%CI: 0.35-1.02; I2= 60.2%; P < 0.001). Conclusions: Cataract surgery is linked to a lower incidence of all-cause dementia and Alzheimer's disease. A cataract is a reversible visual impairment. Cataract surgery may be a protective factor against the onset of all-cause dementia and can reduce the economic and family burden caused by all-cause dementia worldwide. Given the restricted pool of included studies, our findings necessitate meticulous interpretation. Systematic review registration: http://www.crd.york.ac.uk/prospero retrieve registration details by searching CRD4202379371.

Clinical Effect of the Anterior Fascia of Tarsus Tightening Combined With Lower Eyelid Blepharoplasty for Senile Entropion.

OBJECTIVE: A majority of patients with senile entropion have a lower eyelid pouch. This study aimed to explore a modified method to correct the entropion and enhance ophthalmic cosmetology. PATIENTS AND METHODS: Patients with senile entropion and lower eyelid pouches, who underwent anterior fascia of tarsus tightening combined with lower eyelid pouch plastic surgery from 2018 to 2019, were enrolled in the study. The data on operation time, postoperative effect, degree of eyelid swelling after surgery, patient satisfaction, and recurrence rate were recorded. RESULTS: The lower eyelid entropion was well corrected in all of the 46 patients after the surgery, and the lower eyelid pouch and saggy skin were satisfactorily repaired. After 1-year follow-up, no recurrence of lower eyelid eversion and ectropion was observed. The shape of the orbital areas was natural in all the patients, the incision scar was hidden, and the patient achieved a high degree of satisfaction. CONCLUSIONS: In patients with senile entropion and lower eyelid pouch, anterior tarsal fascia tightening combined with lower eyelid blepharoplasty could not only increase the cure rate and reduce the recurrence rate but also achieve good appearance and improve patient satisfaction.

Osthole attenuates pulmonary arterial hypertension by the regulation of sphingosine 1-phosphate in rats.

Osthole is observed to have the capacity to treat pulmonary arterial hypertension (PAH) in rats, but molecular mechanism is still unknown. The present study aims to discover therapeutic targets and explore therapeutic mechanism of osthole against PAH from metabolic perspective. A rat model with PAH was successfully established with MCT, following osthole administration, then untargeted metabolomics assay was performed using UPLC-Q-TOF-MS to identify differential metabolites and associated metabolic pathways, at last mechanism investigation was done by qRT-PCR, Western blot and ELISA. Differential metabolites characterized in rats with PAH were mostly assigned to sphingolipid metabolism, synthesis of unsaturated fatty acids, glycolysis, nucleotide metabolism, steroid hormone biosynthesis. Furthermore, osthole reversed high level of S1P by modulating metabolic enzyme Sphk1 in rats with PAH. In addition, osthole inhibited the expression of Sphk1 by downregulating microRNA-21, phosphorylation of Akt, phosphorylation of mTOR in vivo and in vitro. These results demonstrated that metabolomics is a promising approach to discover potential drug target for PAH treatment. Importantly, our findings further elucidated therapeutic mechanism of osthole, a natural product, having a role of metabolic regulator to potentially treat PAH by targeting inhibition of Sphk1/S1P via microRNA-21-PI3K/Akt/mTOR signal pathway. Altogether, this discovery paves a critical foundation for enabling osthole to be a candidate compound to treat PAH.

Chamaejasmin B Decreases Malignant Characteristics of Mouse Melanoma B16F0 and B16F10 Cells.

Chamaejasmin B (CHB), a natural biflavone isolated from Stellera chamaejasme L., has been reported to exhibit anti-cancer properties; however, its effect in melanoma cells is not clear. Here, we aimed to investigate the anticancer effect of CHB in mouse melanoma B16F0 and B16F10 cells. We found that CHB significantly suppressed cell proliferation and promoted cell cycle arrest at G0/G1 phase in B16F0 cells; it also induced cell differentiation and increased melanin content by increasing tyrosinase (TYR) activity and mRNA levels of melanogenesis-related genes in B16F0 cells. Meanwhile, wound closure, invasion, and migration of B16F0 and B16F10 cells were dramatically inhibited. Moreover, CHB significantly increased ROS levels and decreased ΔΨm, resulting in B16F0 and B16F10 cell apoptosis. Finally, in vivo studies showed that CHB inhibited tumor growth and induced tumor apoptosis in a mouse xenograft model of murine melanoma B16F0 and B16F10 cells. Overall, CHB decreases malignant characteristics and may be a promising therapeutic agent for malignant melanoma cells via multiple signaling pathways.

Function-based high-throughput screening for antibody antagonists and agonists against G protein-coupled receptors.

Hybridoma and phage display are two powerful technologies for isolating target-specific monoclonal antibodies based on the binding. However, for complex membrane proteins, such as G protein-coupled receptors (GPCRs), binding-based screening rarely results in functional antibodies. Here we describe a function-based high-throughput screening method for quickly identifying antibody antagonists and agonists against GPCRs by combining glycosylphosphatidylinositol-anchored antibody cell display with ß-arrestin recruitment-based cell sorting and screening. This method links antibody genotype with phenotype and is applicable to all GPCR targets. We validated this method by identifying a panel of antibody antagonists and an antibody agonist to the human apelin receptor from an immune antibody repertoire. In contrast, we obtained only neutral binders and antibody antagonists from the same repertoire by phage display, suggesting that the new approach described here is more efficient than traditional methods in isolating functional antibodies. This new method may create a new paradigm in antibody drug discovery.

LncRNA Gm2044 promotes 17ß-estradiol synthesis in mpGCs by acting as miR-138-5p sponge.

Long noncoding RNAs (lncRNAs) have been demonstrated to play vital roles in mammalian reproduction. Our previous research revealed that lncRNA Gm2044 is highly expressed in mouse spermatocytes and regulates male germ cell function. The gene annotation database BioGPS shows that Gm2044 is not only highly expressed in testicular tissue but also in ovarian tissue, which suggests that Gm2044 may be involved in female reproductive development. In this study, we confirmed that lncRNA Gm2044 promotes 17ß-estradiol synthesis in mouse pre-antral follicular granulosa cells (mpGCs). Furthermore, bioinformatics methods, western blot, and the luciferase assay proved that Gm2044 functions as a miR-138-5p sponge to inhibit the direct target of miR-138-5p, Nr5a1, which enhances 17ß-estradiol synthesis through cyp19a1 activation. Taken together, our results provide an insight into the mechanistic roles of lncRNA Gm2044 for 17ß-estradiol synthesis by acting as competing-endogenous RNAs to modulate the function of mpGCs. Studying the potential lncRNAs, which regulate estradiol release, will be beneficial for the diagnosis and treatment of steroid hormone-related disease.

Anti-Proliferation and Pro-Apoptotic Effects of Diosmetin via Modulating Cell Cycle Arrest and Mitochondria-Mediated Intrinsic Apoptotic Pathway in MDA-MB-231 Cells.

BACKGROUND Breast cancer is one of the most malignant tumors worldwide. The natural flavonoid diosmetin has been reported to exhibit various pharmacological activities, including anti-cancer effects. This study aimed to investigate the anti-breast cancer effects of diosmetin on MDA-MB-231 cells and to explore the underlying molecular mechanisms of cell apoptosis. MATERIAL AND METHODS The MDA-MB-231 cells were incubated with diosmetin for 24 h. Then, cell viability and lactate dehydrogenase (LDH) leakage were detected using CCK-8 and LDH assay kits, respectively. Inverted fluorescence microscopy and flow cytometry were used to measure the mitochondrial membrane potential (MMP) and intracellular reactive oxygen species (ROS). Cell apoptosis and cell cycle were determined by flow cytometry. The expressions of apoptosis and cell cycle-related genes were determined by Western blotting and qRT-PCR. RESULTS The results revealed that diosmetin exerts significant cytotoxic effects on MDA-MB-231 cells, as indicated by decreased cell viability, increased intracellular ROS accumulation and LDH release, as well as cell cycle arrest in G0/G1 phase, inducing mitochondrial dysfunction and apoptosis. Moreover, diosmetin treatment significantly downregulated the expression levels of Bcl-2 and Cyclin D1, and upregulated that of p53, Bax, caspase 3, cleaved caspase 9, and cleaved caspase 3. CONCLUSIONS These findings demonstrate that diosmetin has anti-proliferative and pro-apoptotic activities against MDA-MB-231 cells via cell cycle arrest and the mitochondria-mediated intrinsic apoptotic pathway. Our results extend the understanding of the anti-tumor mechanism of diosmetin and suggest that it may be of use as an active natural agent for the prevention or treatment of human breast cancer.

Alteronol Enhances the Anti-tumor Activity and Reduces the Toxicity of High-Dose Adriamycin in Breast Cancer.

The first-line chemotherapy drug adriamycin (ADM) is widely used for the treatment of breast cancer, but the acquired drug resistance and the normal tissue toxicity remain clinical challenges. Alteronol has been reported to exert wide-ranging anti-tumor activity. In this study, we firstly examined the synergistic anti-tumor effects and the underlying mechanisms of alteronol combined with ADM in breast cancer. We have found that the combination of alteronol and ADM significantly suppressed the expression levels of the cell cycle-related proteins (CDC2 and Cyclin B1) and induced cell cycle arrest at the G2/M phase, leading to cell proliferation inhibition in breast cancer 4T1 cells. Moreover, co-treatment of alteronol and ADM (i) remarkably activated p38 and JNK kinases, (ii) elevated ROS levels, (iii) triggered mitochondrial dysfunction, (iv) released cytochrome c into the cytoplasm, (v) upregulated apoptosis-related proteins, e.g., cleaved PARP, Bax, and cleaved caspase-3/9, and (vi) downregulated the expression of Bcl-2, followed by apoptosis. Furthermore, our in vivo studies showed that the low-dose combination of alteronol (2 mg/kg) and ADM (1 mg/kg) significantly inhibited tumor growth in tumor bearing mice, and the anti-tumor effect of the combination was the same as that of high-dose ADM (8 mg/kg). In addition, the low-dose combination group showed lower toxicities to major organs than the high-dose ADM group. Taken together, these data demonstrate that the low-dose combination of alteronol and ADM could notably improve the anti-tumor activity and have lower toxicities to major organs than those in high-dose ADM group.

Isoliquiritigenin Induces Mitochondrial Dysfunction and Apoptosis by Inhibiting mitoNEET in a Reactive Oxygen Species-Dependent Manner in A375 Human Melanoma Cells.

The mitochondrial protein mitoNEET is a type of iron-sulfur protein localized to the outer membrane of mitochondria and is involved in a variety of human pathologies including cystic fibrosis, diabetes, muscle atrophy, and neurodegeneration. In the current study, we found that isoliquiritigenin (ISL), one of the components of the root of Glycyrrhiza glabra L., could decrease the expression of mitoNEET in A375 melanoma cells. We also demonstrated that mitoNEET could regulate the content of reactive oxygen species (ROS), by showing that the ISL-mediated increase in the cellular ROS content could be mitigated by the mitoNEET overexpression. We also confirmed the important role of ROS in ISL-treated A375 cells. The increased apoptosis rate and the decreased mitochondrial membrane potential were mitigated by the overexpression of mitoNEET in A375 cells. These findings indicated that ISL could decrease the expression of mitoNEET, which regulated ROS content and subsequently induced mitochondrial dysfunction and apoptosis in A375 cells. Our findings also highlight mitoNEET as a promising mitochondrial target for cancer therapy.

Low Dose of Acacetin Promotes Breast Cancer MCF-7 Cells Proliferation Through the Activation of ERK/ PI3K /AKT and Cyclin Signaling Pathway.

BACKGROUND: Phytoestrogens have been proposed as replaceable medicines for climacteric hormone replacement therapy, on the basis of EP3138562 and US5516528. However, recent studies demonstrated that phytoestrogens might promote the proliferation of breast cancer cells, which is rooted in their estrogenic activity. Acacetin, as one phytoestrogen, has been reported to exhibit estrogenic activity. But the effect of acacetin on breast cancer cells proliferation and its mechanism has not been explored. OBJECTIVE: This study aims to evaluate the effects of acacetin on breast cancer MCF-7 cells proliferation and to explore its possible mechanism. METHODS: Sulforhodamine B (SRB) assay was used to test the proliferation rate of MCF-7 cells. Flow cytometry was utilized to determine cell cycle. RT-qPCR and western blot were employed to evaluate the expressions of proliferation-related factors in mRNA and protein levels. RESULTS: According to SRB assay and flow cytometric analysis, low dose of acacetin from 10-3 to 1µM promoted the MCF-7 cells proliferation in a dose-dependent and time-dependent manner. Moreover, the expressions of cell cycle-related molecules, ERK1/2 and PI3K/AKT were increased after treatment with acacetin, while the increases were effectively reversed by ER antagonist ICI 182,780. Further studies showed that acacetin notably induced increasing mRNA and proteins levels of ERα, which were strongly reversed by ERα antagonist MPP. CONCLUSION: Low dose of acacetin from 10-3 µM to µM promoted the proliferation of MCF-7 cells through the ERK/PI3K/AKT pathway and its downstream cyclin signaling. And ERα is mainly responsible for acacetin promoting proliferation in MCF-7 cells.

Licochalcone D induces apoptosis and inhibits migration and invasion in human melanoma A375 cells.

The aim of the present study was to determine the effects of Licochalcone D (LD) on the apoptosis and migration and invasion in human melanoma A375 cells. Cell proliferation was determined by sulforhodamine B assay. Apoptosis was assessed by Hoechst 33258 and Annexin V­FITC/PI staining and JC­1 assay. Total intracellular reactive oxygen species (ROS) was examined by DCFH­DA. Wound healing and Transwell assays were used to detect migration and invasion of the cells. The activities of matrix metalloproteinase (MMP­2 and MMP­9) were assessed via gelatin zymography. Tumor growth in vivo was evaluated in C57BL/6 mice. RT­PCR, qPCR, ELISA and western blot analysis were utilized to measure the mRNA and protein levels. Our results showed that LD inhibited the proliferation of A375 and SK­MEL­5 cells in a concentration­dependent manner. After treatment with LD, A375 cells displayed obvious apoptotic characteristics, and the number of apoptotic cells was significantly increased. Pro­apoptotic protein Bax, caspase­9 and caspase­3 were upregulated, while anti­apoptotic protein Bcl­2 was downregulated in the LD­treated cells. Meanwhile, LD induced the loss of mitochondrial membrane potential (ΔΨm) and increased the level of ROS. ROS production was inhibited by the co­treatment of LD and free radical scavenger N­acetyl­cysteine (NAC). Furthermore, LD also blocked A375 cell migration and invasion in vitro which was associated with the downregulation of MMP­9 and MMP­2. Finally, intragastric administration of LD suppressed tumor growth in the mouse xenograft model of murine melanoma B16F0 cells. These results suggest that LD may be a potential drug for human melanoma treatment by inhibiting proliferation, inducing apoptosis via the mitochondrial pathway and blocking cell migration and invasion.

Exploring the Biocompatibility of Zwitterionic Copolymers for Controlling Macrophage Phagocytosis of Bacteria.

This paper provides a biomaterial derived from zwitterionic polymer for controlling macrophage phagocytosis of bacteria. A series of zwitterionic copolymers, named DMAPS-co-AA, are synthesized with 3-dimethyl (methacryloyloxyethyl) ammonium propane sulfonate (DMAPS) and acrylic acid (AA). The biocompatibility of DMAPS-co-AA copolymers can be adjusted by adjusting the DMAPS-content or pH value. As the DMAPS-content increases, the biocompatibility of zwitterionic copolymer increases. The zwitterionic copolymers with DMAPS content above 30 wt% have higher biocompatibility. Moreover, the biocompatibility also increases significantly as the pH increases from 3.4 to 7.2. By adjusting the pH above 5.8, the zwitterionic copolymer with lower DMAPS-content also shows higher biocompatibility. Importantly, after incubation with the DMAPS-co-AA copolymer solutions at different pH values, phagocytosis behavior of macrophage RAW264.7 cells can also be adjusted. The phagocytosis of bacteria is enhanced at pH = 7.2. Thus, it is proposed that zwitterionic copolymers can be used for controlling phagocytosis of bacteria.

Neuroprotective Effect of Scutellarin on Ischemic Cerebral Injury by Down-Regulating the Expression of Angiotensin-Converting Enzyme and AT1 Receptor.

BACKGROUND AND PURPOSE: Previous studies have demonstrated that angiotensin-converting enzyme (ACE) is involved in brain ischemic injury. In the present study, we investigated whether Scutellarin (Scu) exerts neuroprotective effects by down-regulating the Expression of Angiotensin-Converting Enzyme and AT1 receptor in a rat model of permanent focal cerebral ischemia. METHODS: Adult Sprague-Dawley rats were administrated with different dosages of Scu by oral gavage for 7 days and underwent permanent middle cerebral artery occlusion (pMCAO). Blood pressure was measured 7 days after Scu administration and 24 h after pMCAO surgery by using a noninvasive tail cuff method. Cerebral blood flow (CBF) was determined by Laser Doppler perfusion monitor and the neuronal dysfunction was evaluated by analysis of neurological deficits before being sacrificed at 24 h after pMCAO. Histopathological change, cell apoptosis and infarct area were respectively determined by hematoxylin-eosin staining, terminal deoxynucleotidyl transfer-mediated dUTP nick end labeling (TUNEL) analysis and 2,3,5-triphenyltetrazolium chloride staining. Tissue angiotensin II (Ang II) and ACE activity were detected by enzyme-linked immunosorbent assays. The expression levels of ACE, Ang II type 1 receptor (AT1R), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1ß (IL-1ß) were measured by Western blot and real-time PCR. ACE inhibitory activity of Scu in vitro was detected by the photometric determination. RESULTS: Scu treatment dose-dependently decreased neurological deficit score, infarct area, cell apoptosis and morphological changes induced by pMCAO, which were associated with reductions of ACE and AT1R expression and the levels of Ang II, TNF-α, IL-6, and IL-1ß in ischemic brains. Scu has a potent ACE inhibiting activity. CONCLUSION: Scu protects brain from acute ischemic injury probably through its inhibitory effect on the ACE/Ang II/AT1 axis, CBF preservation and proinflammation inhibition.

Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart.

This study aims to evaluate the cardioprotective effects of astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague-Dawley rats were randomly divided into five groups. The results showed that astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) decreased in astragalin-treated groups. The infarct size (IS) and apoptosis rate in hearts from astragalin-treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that astragalin preconditioning significantly reduced Bax level, whereas Bcl-2 was increased in the myocardium. Therefore, astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti-inflammatory activities.

Protective Effects of Kaempferol against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart via Antioxidant Activity and Inhibition of Glycogen Synthase Kinase-3ß.

OBJECTIVE: This study aimed to evaluate the protective effect of kaempferol against myocardial ischemia/reperfusion (I/R) injury in rats. METHOD: Left ventricular developed pressure (LVDP) and its maximum up/down rate (±dp/dt max) were recorded as myocardial function. Infarct size was detected with 2,3,5-triphenyltetrazolium chloride staining. Cardiomyocyte apoptosis was determined using terminal deoxynucleotidyl nick-end labeling (TUNEL). The levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined using enzyme linked immunosorbent assay (ELISA). Moreover, total glycogen synthase kinase-3ß (GSK-3ß), phospho-GSK-3ß (P-GSK-3ß), precaspase-3, cleaved caspase-3, and cytoplasm cytochrome C were assayed using Western blot analysis. RESULTS: Pretreatment with kaempferol significantly improved the recovery of LVDP and ±dp/dt max, as well as increased the levels of SOD and P-GSK-3ß and GSH/GSSG ratio. However, the pretreatment reduced myocardial infarct size and TUNEL-positive cell rate, as well as decreased the levels of cleaved caspase-3, cytoplasm cytochrome C, CK, LDH, MDA, and TNF-α. CONCLUSION: These results suggested that kaempferol provides cardioprotection via antioxidant activity and inhibition of GSK-3ß activity in rats with I/R.

Role of licochalcone C in cardioprotection against ischemia/reperfusion injury of isolated rat heart via antioxidant, anti-inflammatory, and anti-apoptotic activities.

AIMS: This study aimed to evaluate the protective effect of licochalcone C against myocardial ischemia/reperfusion injury in rats. MAIN METHODS: Left ventricular developed pressure (LVDP) and its maximum up/down rate (±dp/dtmax) were recorded as myocardial function. Levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined by using enzyme-linked immunosorbent assay. Cell morphology was observed and mitochondrial damage was assessed by HE coloration and transmission electron microscopy, respectively. Cardiomyocyte apoptosis was determined by using terminal deoxynucleotidyl transferased UTP nick-end labeling (TUNEL). KEY FINDINGS: Pretreatment with licochalcone C significantly improved the recovery of LVDP and ±dp/dtmax, and increased the levels of SOD and GSH/GSSG ratio. However, pretreatment with licochalcone C not only decreased the TUNEL-positive cell ratio and morphological changes, but also weaken the mitochondrial injury and the levels of CK, LDH, MDA, and TNF-α. SIGNIFICANCE: These results suggested an important function of licochalcone C extracted from traditional Chinese medicine in the cardioprotection via antioxidant, anti-inflammatory, and anti-apoptotic activities.