Stabilizing Decavanadate Cluster as Electrode Material in Sodium and Lithium-ion Batteries.

Decavanadate ([V10 O28 ]6- , {V10 }) clusters are a potential electrode material for lithium and post-lithium batteries; however, their low stability due to the solubility in liquid organic electrolytes has been challenging. These molecular clusters are also prone to transform into solid-state oxides at a moderate temperature needed in the typical electrode fabrication process. Hence, controlling the solubility and improving the thermal stability of compounds are essential to make them more viable options for use as battery electrodes. This study shows a crystal engineering approach to stabilize the cluster with organic guanidinium (Gdm+ ) cation through the hydrogen-bonding interactions between the amino groups of the cation and the anion. The comparison of solubility and thermal stability of the Gdm{V10 } with another cluster bearing tetrabutylammonium (Tba+ ) cation reveals the better stability of cation-anion assembly in the former than the latter. As a result, the Gdm{V10 } delivers better rate capability and cycling stability than Tba{V10 } when tested as anode material in a half-cell configuration of a sodium-ion battery. Finally, the performance of the Gdm{V10 } anode is also investigated in a lithium-ion battery full cell with LiFePO4 cathode.

Amelioration of CCl4-induced oxidative stress and hepatotoxicity by Ganoderma lucidum in long evans rats.

Liver disease is a serious health problem affecting people worldwide at an alarming rate. The present study aimed to investigate the protective effects of Ganoderma lucidum against CCl4-induced liver toxicity in rats. The experimental Long Evans rats were divided into five groups, of which four groups were treated with carbon tetrachloride (CCl4). Among the CCl4 treated groups, one of the groups was treated with silymarin and two of them with ethanolic extract of G. lucidum at 100 and 200 mg/Kg body weight. The oxidative stress parameters and endogenous antioxidant enzyme concentrations were assessed by biochemical tests. Liver enzymes ALT, AST, and ALP were determined spectrophotometrically. Histopathological examinations were carried out to assess hepatic tissue damage and fibrosis. Reverse transcription PCR (RT-PCR) was performed to determine the expression of IL-1ß, IL-6, IL-10, TNF-α, and TGF-ß genes. Gas Chromatography-Mass Spectroscopy (GC-MS) analysis revealed that G. lucidum is rich in several phytochemicals including 6-Octadecanoic acid (55.81%), l-( +)-Ascorbic acid 2,6-dihexadecanoate (18.72%), Cis-11-Eicosenamide (5.76%), and Octadecanoic acid (5.26%). Treatment with the G. lucidum extract reduced the elevated ALT, AST, ALP levels, and cellular oxidative stress markers and increased the endogenous antioxidant levels. Histopathology observations revealed that the inflammation, infiltration of immune cells, and aberration of collagen fibers in the hepatocytes were altered by the G. lucidum treatment. The increased expression of inflammatory cytokines TNF-α, TGF-ß, IL-1 ß, and IL-6 were markedly suppressed by G. lucidum extract treatment. G. lucidum also prevented the suppression of protective IL-10 expression by CCl4. This study strongly suggests that G. lucidum extract possesses significant hepatoprotective activity as evidenced by reduced oxidative stress and inflammation mediated by suppression in inflammatory cytokine expression and increased protective IL-10 cytokine expression.

Evaluation of Total Phenolic Content, HPLC Analysis, and Antioxidant Potential of Three Local Varieties of Mushroom: A Comparative Study.

Functional foods such as mushrooms are rich in polyphenolic compounds and secondary metabolites with health-promoting properties such as antioxidant, antimicrobial, antidiabetic and immunostimulatory effects. The present study is aimed to investigate the ethanolic extracts of three varieties of mushrooms, namely, G. lucidum, G. tropicum, and C. indica grown in Bangladesh for phenolic and flavonoid content and their antioxidant properties. Moreover, the phenolic composition of the extracts was analyzed by using the HPLC-DAD system. G. lucidum extract exhibited the highest antioxidant potential as evidenced by its lowest IC50 value in all the tested assay models (40.44 ± 2.09 µg/mL, 151.32 ± 0.35 µg/mL, 137.89 ± 1.85 µg/mL in DPPH, H2O2, and NO scavenging assay, respectively) along with the highest phenolic content (81.34 ± 0.68 GAE g-1 extract). G. tropicum and C. indica extracts also showed significant antioxidant properties and a good amount of phenolic content, 52.16 ± 0.25 GAE g-1 extract, and 47.1 ± 0.26 GAE g-1 extract, respectively. The scavenging activity increased with the increasing concentration of extracts in all cases. The total phenolic content of the ethanolic extracts of mushroom species was highly correlated with antioxidant effects with Pearson's correlation coefficient (r) values ranging from 0.8883-0.9851. The α-amylase inhibitory and antibacterial activity of G. lucidum was evaluated by using 3,5-dinitrosalicylic acid and disc diffusion method, respectively. The maximum inhibitory activity recorded against α-amylase was 70.98 ± 0.042% at a concentration of 500 µg/mL. G. lucidum extract exhibited the highest antibacterial activity against Pseudomonas aeruginosa with 23.00 ± 1.00 mm clear zone of inhibition and an MIC value of 3.5 mg/mL. The results indicate that the mushroom species tested in this study could serve as a potential source of natural antioxidants in the development of nutraceuticals and herbal drugs for the management of oxidative stress-associated diseases as well as infectious diseases.

Cellular senescence and its impact on the circadian clock.

Ageing is one of the greatest risk factors for chronic non-communicable diseases, and cellular senescence is one of the major causes of ageing and age-related diseases. The persistent presence of senescent cells in late life seems to cause disarray in a tissue-specific manner. Ageing disrupts the circadian clock system, which results in the development of many age-related diseases such as metabolic syndrome, cancer, cardiac diseases and sleep disorders and an increased susceptibility to infections. In this review, we first discuss cellular senescence and some of its basic characteristics and detrimental roles. Then, we discuss a relatively unexplored topic on the link between cellular senescence and the circadian clock and attempt to determine whether cellular senescence could be the underlying factor for circadian clock disruption.

Cellular Senescence Triggers Altered Circadian Clocks With a Prolonged Period and Delayed Phases.

Senescent cells, which show the permanent growth arrest in response to various forms of stress, accumulate in the body with the progression of age, and are associated with aging and age-associated diseases. Although the senescent cells are growth arrested, they still demonstrate high metabolic rate and altered gene expressions, indicating that senescent cells are still active. We recently showed that the circadian clock properties, namely phase and period of the cells, are altered with the establishment of replicative senescence. However, whether cellular senescence triggers the alteration of circadian clock properties in the cells is still unknown. In this study we show that the oxidative stress-induced premature senescence induces the alterations of the circadian clock, similar to the phenotypes of the replicative senescent cells. We found that the oxidative stress-induced premature senescent cells display the prolonged period and delayed phases. In addition, the magnitude of these changes intensified over time, indicating that cellular senescence changes the circadian clock properties. Our current results corroborate with our previous findings and further confirm that cellular senescence induces altered circadian clock properties, irrespective of the replicative senescence or the stress-induced premature senescence.

Over-expression of Nicotinamide phosphoribosyltransferase in mouse cells confers protective effect against oxidative and ER stress-induced premature senescence.

A main feature of aged organisms is the accumulation of senescent cells. Accumulated senescent cells, especially stress-induced premature senescent cells, in aged organisms lead to the decline of the regenerative potential and function of tissues. We recently reported that the over-expression of NAMPT, which is the rate-limiting enzyme in mammalian NAD+ salvage pathway, delays replicative senescence in vitro. However, whether Nampt-overexpressing cells are tolerant of stress-induced premature senescence remains unknown. Here, we show that primary mouse embryonic fibroblasts derived from Nampt-overexpressing transgenic mice (Nampt Tg-MEF cells) possess resistance against stress-induced premature senescence in vitro. We found that higher oxidative or endoplasmic reticulum (ER) stress is required to induce premature senescence in Nampt Tg-MEF cells compared to wild-type cells. Moreover, we found that Nampt Tg-MEF cells show acute expression of unfolded protein response (UPR)-related genes, which in turn would have helped to restore proteostasis and avoid cellular senescence. Our results demonstrate that NAMPT/NAD+ axis functions to protect cells not only from replicative senescence, but also from stress-induced premature senescence in vitro. We anticipate that in vivo activation of NAMPT activity or increment of NAD+ would protect tissues from the accumulation of premature senescent cells, thereby maintaining healthy aging.

Replicative senescent human cells possess altered circadian clocks with a prolonged period and delayed peak-time.

Over the last decade, a wide array of evidence has been accumulated that disruption of circadian clock is prone to cause age-related diseases and premature aging. On the other hand, aging has been identified as one of the risk factors linked to the alteration of circadian clock. These evidences suggest that the processes of aging and circadian clock feedback on each other at the animal level. However, at the cellular level, we recently revealed that the primary fibroblast cells derived from Bmal1-/- mouse embryo, in which circadian clock is completely disrupted, do not demonstrate the acceleration of cellular aging, i.e., cellular senescence. In addition, little is known about the impact of cellular senescence on circadian clock. In this study, we show for the first time that senescent cells possess a longer circadian period with delayed peak-time and that the variability in peak-time is wider in the senescent cells compared to their proliferative counterparts, indicating that senescent cells show alterations of circadian clock. We, furthermore, propose that investigation at cellular level is a powerful and useful approach to dissect molecular mechanisms of aging in the circadian clock.