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Here, we report the central role of predicted Ca2+-binding site 1 within the hinge region of the extracellular domain (ECD) of CaSR and its interaction with. Our results indicated that gentamicin could decrease cell viability, increase cytotoxicity, stimulate ROS generation, reduce mitochondrial.

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Abstract Metabotropic glutamate receptors (mGluRs) and calcium receptors (CaR) are closely related G protein‐coupled receptors (GPCRs). Entomopathogenic nematodes (EPNs) provide a potential alternative to chemical insecticides to control root-feeding pests of agricultural and forestry crops. One. Our LC/MS and NMR data showed that positions 6 and 8 of the EGCG A-ring were the major active sites for trapping reactive dicarbonyl compounds. The objective of this work was to evaluate the effect of physical modification of potato starch by gelatinization, spray-freezing on liquid nitrogen and. Thank you to Dr. Jin Zou for teach- ing me protein engineering and related biophysical assays, Dr. Mulpuri Nagaraju for helping MD simulation and.

Nian Nian You Yu brabet

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Or enter first few letters:. Sort by: title issue date submit date Order: ascending descending Results: 5 10 20 40 60 80 JavaScript is disabled for your browser. Some features of this site may not work without it. Many low-middle income countries in Africa have poorly-developed infectious disease monitoring systems. Entomopathogenic nematodes EPNs provide a potential alternative to chemical insecticides to control root-feeding pests of agricultural and forestry crops. One of the challenges in using EPNs in these environments is low

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Federal government websites often end in. The site is secure. Excessive levels of reactive oxygen species ROS lead to mitochondrial damage and apoptotic cell death in gentamicin-induced ototoxicity. However, its protective effect on gentamicin-induced ototoxicity remains unexplored. We evaluated the effect of gentamicin and THSG on the ROS level, superoxide dismutase SOD activity, mitochondrial membrane potential, nuclear condensation, and lactate dehydrogenase LDH release, and the expression of apoptosis-related proteins was assessed to understand the molecular mechanisms underlying its preventive effects.

However, THSG treatment reversed these effects by suppressing ROS production and downregulating the mitochondrial-dependent apoptotic pathway. Additionally, it increased the SOD activity, decreased the expression of apoptosis-related proteins, alleviated the levels of the apoptotic cells, and impaired cytotoxicity.

To the best of our knowledge, this is the first study to demonstrate that THSG could be a potential therapeutic option to attenuate gentamicin-induced ototoxicity. The World Health Organization has estimated that there are about million people approximately 6. Hearing loss can occur due to aging, noise exposure, and ototoxic drugs e. Cochleae are vulnerable to oxidative stress on account of the high metabolic demands of hair cells in reaction to stimulation [ 5 ]. Moreover, ROS contribute to cellular dysfunction, including DNA damage and lipid peroxidation, leading to cochlear degeneration [ 6 ].

Gentamicin, an aminoglycoside antibiotic, is commonly used to treat infections caused by aerobic Gram-negative and some Gram-positive bacteria [ 7 ]. Mechanistically, the ototoxic effects of gentamicin are mediated by the oxidative stress pathway [ 9 , 10 ], apoptosis [ 11 , 12 , 13 ], autophagy [ 14 , 15 ], and the Akt survival pathway [ 16 , 17 , 18 ].

Apoptosis plays an important role in maintaining intracellular homeostasis and participates in the pathogenesis of hearing loss [ 19 ]. Excessive ROS production by ototoxic drugs is associated with hair cell damage via the apoptotic pathway [ 20 ]. In addition, it has been shown that antioxidants attenuated gentamicin-induced hair cell damage, suggesting a possible relationship between ROS and gentamicin-induced ototoxicity [ 21 ]. Polygonum multiflorum Thunb. It is also used in medicinal food to improve health.

In addition, it has also been shown that THSG improves blood flow and ameliorates vascular senescence in spontaneously hypertensive rats [ 30 ]. Moreover, recent studies have reported the protective effect of THSG on oxidative stress-induced cellular damage.

However, the relationship between gentamicin ototoxicity and THSG remains unknown. In this study, we investigated the otoprotective effect of THSG in the gentamicin-treated mouse cochlear cell line and elucidated the molecular mechanisms underlying the protective effects of THSG.

The findings demonstrated the potential of THSG to treat gentamicin-induced ototoxicity. The assessment of cell viability showed that gentamicin inhibited the cell viability in a dose-dependent manner. As shown in Figure 1 B, gentamicin significantly increased the release of LDH in a dose-dependent manner.

The damage to the cells at various gentamicin concentrations 48 h was assessed by A 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide MTT assay and B lactate dehydrogenase LDH release assay. In order to elucidate the mechanisms involved in the toxic effect of gentamicin via activation of apoptosis, we detected the relative expression of cleaved poly ADP-ribose polymerase PARP , an indicator of apoptosis.

As shown in Figure 1 C,D, the relative expression levels of cleaved PARP were significantly increased after gentamicin treatment in a time-dependent and dose-dependent manner. The fluorescence signal intensity of DCFDA staining was boosted in the gentamicin-treated group compared to the untreated group.

JC-1 dye produces orange-red fluorescence in healthy mitochondria but green fluorescence at low membrane potential. As shown in Figure 3 A, the gentamicin only group displayed a relatively low ratio of red to green fluorescence. The THSG in gentamicin-treated groups exhibited an increased ratio of red to green fluorescence compared to the gentamicin-alone group. The results showed that THSG recovered the gentamicin-induced loss of mitochondrial membrane potential.

As cytochrome c is a key mediator of the apoptosis pathway, we next evaluated the gentamicin-stimulated cytochrome c release from mitochondria. Images were obtained under a fluorescence microscope. B Cytochrome c was analyzed by western blotting in cytosolic and mitochondrial fractions. To confirm the apoptotic effects of THSG on mitochondrial-dependent apoptosis, the protein expression of cleaved caspase 9, cleaved caspase 3, and cleaved PARP were analyzed by western blotting.

Additionally, the nuclear staining using Hoechst dye showed a lower fluorescence intensity of Hoechst in the THSG-treated groups than in the gentamicin-alone group Figure 4 B indicating reduced nuclear condensation. A Protein levels of cleaved caspase 9, cleaved caspase 3, and cleaved PARP were analyzed by western blotting. B Nuclear apoptotic changes were assessed using Hoechst fluorescence dye. Images were obtained using a fluorescence microscope. We analyzed the population of apoptotic cells using Annexin V and propidium iodide PI double staining.

The results revealed that the percentage of apoptosis was significantly lower in the THSG-treated groups as compared to the gentamicin-alone group Figure 5 A. B Cytotoxicity was monitored by measuring LDH release. These results suggested that THSG could attenuate the cochlear cell damage caused by gentamicin. In biomedical research, cell lines are used as models for various purposes in vitro. In , Hata et al.

Several studies have demonstrated the antioxidative capacity of THSG [ 25 ], and its antioxidant potential could be ascribed to its hydroxyl groups [ 40 ]. Lin et al. Our previous study reported that THSG has free radical scavengers and activates the Nrf2 signaling pathway to mitigate H 2 O 2 -induced ototoxicity [ 31 ]. However, future investigations are required to better clarify the antioxidant properties of THSG in oxidative stress-induced damage and the protective effects of THSG from drug-induced ototoxicity.

Aminoglycoside antibiotics are used widely for the treatment of bacterial infections because of their effectiveness and lower drug prices.

However, the use of these agents is limited by their side effects, such as ototoxicity and nephrotoxicity [ 8 ]. Moreover, ROS formation has been shown to be related to aminoglycoside antibiotics-induced hair cell damage [ 44 ]. Therefore, co-administration of an aminoglycoside antibiotic and an antioxidant agent has been developed as a novel therapeutic approach for reducing aminoglycoside-induced ototoxicity at low cost without compromising the antimicrobial activity.

Apoptosis has been conceded to be an important part of aminoglycoside-induced ototoxicity [ 45 ]. Deregulation of apoptosis can contribute to protecting hair cells from ototoxicity [ 20 ]. Gentamicin is one of the most commonly used antibiotics that has been reported to cause vestibular dysfunction and cochlear damage, which may result in balance disorders, tinnitus, and hearing loss [ 4 ].

According to the previous study of El Mouedden et al. Excess ROS levels may contribute to mitochondrial damage, including impairment of RNA translation, protein synthesis, and mitochondrial membrane permeability, and cause mitochondrial-dependent apoptosis [ 49 , 50 , 51 ]. The present study depicts early ROS production in gentamicin-induced toxicity that could have been triggered by lysosomal membrane permeabilization, followed by mitochondrial dysfunction [ 52 ].

Studies have shown that gentamicin causes apoptosis through the mitochondrial-dependent intrinsic apoptotic pathway but not the extrinsic apoptotic pathway [ 53 , 54 , 55 ]. Furthermore, cytochrome c , a caspase activator, is used to characterize the mitochondrial-dependent apoptotic pathway when released from mitochondria to cytosol, followed by the activation of caspase 9, caspase 3, and PARP.

Apoptotic cells show conspicuous changes like nuclear condensation, cell shrinkage, membrane blebbing, and DNA fragmentation. Moreover, we observed that THSG decreased the level of apoptotic cells and cytotoxicity in gentamicin-induced cell damage Figure 5. THSG treatment impairs gentamicin-induced apoptosis by reducing ROS production, stabilizing mitochondrial membrane potential, and downregulating mitochondrial-dependent apoptotic protein expression.

The membranes were incubated with HRP-conjugated secondary antibodies for 1 h at room temperature. Subsequently, protein signal was developed by using enhanced chemiluminescence Bio-Rad Laboratories, Inc. The cell pellet was resuspended in 0. The absorbance was measured at nm.

Fluorescence images were obtained using an Olympus BX41 microscope Tokyo, Japan at the excitation wavelength of nm.

Fluorescence images were obtained using an Olympus BX41 microscope at the excitation wavelength of nm. The cells were harvested and resuspended in a buffer containing 0. The same amount of buffer containing 0. The pellets were resuspended in a buffer containing 0.

A p -value of less than 0. In summary, this study, to the best of our knowledge, is the first to demonstrate that THSG provides significant protection from gentamicin-induced ototoxicity. Treatment with THSG counteracted gentamicin-induced cytotoxicity and apoptosis through reduction of ROS production, stabilization of mitochondrial membrane potential, downregulation of mitochondrial-dependent apoptosis-related proteins, and upregulation of SOD activity.

These findings suggest that THSG could be a potential therapeutic option for the prevention of ototoxicity after gentamicin exposure or as a potential food supplement with antioxidant effects to reduce the prevalence of hearing loss. Conceptualization, Y. All authors have read and agreed to the published version of the manuscript. Sample Availability: Samples of the compounds are not available from the authors. As a library, NLM provides access to scientific literature.

Published online Jul 6. Find articles by Jia-Ni Lin. Received Jun 16; Accepted Jul 5. Abstract Excessive levels of reactive oxygen species ROS lead to mitochondrial damage and apoptotic cell death in gentamicin-induced ototoxicity.

Introduction The World Health Organization has estimated that there are about million people approximately 6. Results 2. Open in a separate window. Figure 1. Figure 2. Figure 3. Figure 4. Figure 5.

Figure 6. Materials and Methods 4. Conclusions In summary, this study, to the best of our knowledge, is the first to demonstrate that THSG provides significant protection from gentamicin-induced ototoxicity.

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Our results indicated that gentamicin could decrease cell viability, increase cytotoxicity, stimulate ROS generation, reduce mitochondrial.

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Sim. Our results indicated that gentamicin could decrease cell viability, increase cytotoxicity, stimulate ROS generation, reduce mitochondrial.

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