Objective This study aimed to examine the impact of riboflavin (RF) on tumor necrosis factor-alpha (TNF-α), caspase-3 (Cas-3) expression, and Sirtuin1 (SIRT1)/protein 53 (p53)/Bcl-2-associated X protein (Bax)/B-cell lymphoma gene-2 (Bcl-2) gene expressions in the diatrizoate (DTZ)-induced experimental nephropathy model. Methods Within the scope of the study, 32 Wistar Albino-type female rats were divided into 4 groups (n = 8). The groups were as follows: Control, DTZ (Rats were given 1 ml saline (SF) by oral gavage for three days. On the third day, intraperitoneal 10 ml/kg and 2.5-3 ml in volume of Urografin in a single dose), DTZ + RF (Rats were given 100 mg/kg RF by oral gavage for three days. On the third day, intraperitoneal 10 ml/kg and 2.5-3 ml of Urografin in a single dose) and RF (Rats were given 100 mg/kg RF by oral gavage for three days. On the third day, intraperitoneal 2.5-3 ml of SF in a single dose). Histopathological, immunohistochemical (TNF-α, Cas-3), biochemical (total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), urea and creatinine), and genetic (SIRT1, p53, Bax, Bcl-2) analyses were performed on the kidney tissues. Results In the DTZ group, pathologic changes, TNF-α and Cas-3 expressions, TOS, OSI, urea, and creatinine levels, p53, and Bax gene expressions increased, while biochemical TAS levels, genetic SIRT1 and Bcl-2 gene expressions decreased. It was determined that these findings observed in the DTZ group were reversed with RF treatment. Conclusions All these results suggest that DTZ-induced renal damage develops through oxidative stress, inflammation, and apoptosis mechanisms and that RF administration can protect renal function by suppressing these processes.

Investigation of potential mechanisms of chronic copper effects on reproduction in zebrafish (Danio rerio).

Rutin (Vitamin P) attenuates oxidative stress, modulates cytokine profile, and preserves alveolar bone microarchitecture and density in a rat periodontitis model.

Prevalence and multidimensional impact of sarcopenia in schizophrenia: Associations with oxidative stress, functioning, and symptom severity.

Prophylactic isoimperatorin protects against LPS-ALI via mTOR-dependent control of inflammation, oxidative stress and ferroptosis markers.

Effect and mechanism of Ganoderma leucocontextum extract on cadmium-toxic nephropathy.

β-Sitosterol attenuates gentamicin-induced nephrotoxicity via ADAM-17/ACE2/Ang 1-7/MasR Axis modulation in rats.

Parental glyphosate exposure primes tomato offspring for enhanced growth and stress tolerance.

Assessment of p-phenylenediamine toxicity in subcellular compartments of hepatic and ocular tissues in Oreochromis mossambicus (Peters, 1852).

Quercetin enhances antioxidant defense and modulates immune homeostasis in mandarin fish (Siniperca chuatsi): Insights from biochemical and transcriptomic analyses.

Effects of PFOA and emerging alternatives at environmental concentrations on murine- and human-derived microglia: A comparative study.

A mixed levan fructan from Rohdea japonica mitigates ulcerative colitis induced by dextran sulfate sodium via regulating intestinal microbiota mediated pyroptosis.

Lipidome changes indicate oxidative stress, inflammation, and specific loss of glycerophosphoserine inflammatory protection in patients with lupus.

Ulcerative Colitis (UC) is a chronic condition characterized by damage to the intestinal mucosal barrier, resulting in bleeding, increased oxidative stress, persistent inflammation, and immune dysregulation. Lotus Leaf (LL), recognized for its dual role as both food and medicine, has demonstrated significant antioxidant and anti-inflammatory properties. Furthermore, its calcined derivative, Lotus Leaf Charcoal (LLC), enhances its astringent, hemostatic, and antidiarrheal effects, positioning it as a promising candidate for the management of UC in both dietary and medicinal contexts. This study aims to explore the potential of LLC in the treatment of UC and its material basis. LLC was prepared by simulating traditional calcination processes through high-temperature pyrolysis at 450 °C, and it was found to contain a large number of spherical nanoparticles uniformly distributed in the range of 0.5-3 nm, exhibiting good dispersibility and stability. In vitro and in vivo experiments demonstrate that LLC exhibits a dose-dependent hemostatic effect which significantly increases platelet (PLT) count, elevates fibrinogen (FIB) concentration, and shortens activated partial thromboplastin time (APTT) and thrombin time (TT). Additionally, LLC shows excellent free radical scavenging abilities against DPPH•, ABTS+•, •OH, and O2-• radicals. Furthermore, LLC exhibits remarkable gastrointestinal stability and long-term retention. In the dextran sulfate sodium (DSS)-induced mouse model of UC, LLC significantly alleviates weight loss, reduces the disease activity index (DAI) and colonic mucosal injury index (CMDI), improves colonic shortening and tissue pathological damage. It downregulates the levels of pro-inflammatory factors such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), decreases indicators of oxidative stress like reactive oxygen species (ROS) and malondialdehyde (MDA), and may inhibit pyroptosis of colonic epithelial cells by suppressing the excessive activation of the NLRP3/Caspase-1/GSDMD signaling pathway. Additionally, it modulates the ratio of CD4+/CD8+ T cells and the Th17/Treg balance in the spleen, thereby restoring immune homeostasis. Additionally, LLC upregulates the expression of tight junction proteins Claudin-1 and Occludin, promoting intestinal barrier repair, and increases the abundance of beneficial bacteria while inhibiting the proliferation of harmful bacteria, ultimately reshaping the intestinal microbiota structure. In summary, LLC contains a substantial amount of carbon nanodots, which improve UC through multiple mechanisms, including mucosal repair, hemostasis, antioxidant effects, anti-inflammatory actions, pyroptosis inhibition, immune modulation, and microbiota regulation. These findings provide a preclinical foundation for developing carbon-based therapeutics for UC.

Purinergic signaling and energetic metabolism in bipolar disorder: From pathophysiology to precision therapeutics.

Mailuo Shutong Pill ameliorates diabetic foot ulcers in rats by suppressing ferroptosis induced by lipid peroxidation.

Schizophrenia is known to be associated with premature mortality. Oxidative stress and telomere maintenance gene polymorphisms are assumed to be the possible trait markers. Hence, the present study aimed to explore the relationship between leukocyte telomere length (LTL) with oxidative stress status and single nucleotide polymorphisms (SNPs) of TERT, TERC, and MYNN genes in patients suffering from schizophrenia. A total of 150 schizophrenia patients and 139 healthy volunteers were recruited. The participants had their LTL measured and TERT rs33954691, TERC rs2293607, and MYNN rs10936599 were genotyped. Oxidative stress index (OSI) based on the ratio of total oxidant status (TOS) to total antioxidant capacity (TAC) was calculated. We found that patients had significantly decreased relative LTL (p = 0.006), but there were no significant effects of oxidative stress level (p = 0.496 for TOS; p = 0.216 for TAC; p = 0.905 for OSI) on relative LTL in schizophrenia. We also confirmed the association between rs33954691 CC (p = 0.007), rs2293607 AG (p = 0.042), and rs10936599 CC (p = 0.001) genotypes and shortened relative LTL in patients with schizophrenia. Thus, the findings suggested the presence of accelerated biological aging in patients with schizophrenia, despite their chronological ages and oxidative stress status. In conclusion, gene polymorphisms may have varying effects on LTL. To further understand the telomere shortening in schizophrenia, baseline and repeated LTL should be investigated.

Epileptic seizures are linked to significant neurochemical, oxidative, inflammatory, and structural changes in the brain, especially within the prefrontal cortex, a region essential for cognition and behaviour. Oxidative stress and neuroinflammation are essential factors in seizure-induced neurodegeneration. Aframomum melegueta, a medicinal plant abundant in bioactive phytochemicals, has exhibited antioxidant and neuroprotective activities; nevertheless, its impact on prefrontal cortical damage subsequent to epilepsy is little defined. This study assessed the impact of Aframomum melegueta on behavioural, biochemical, neurochemical, histological, and inflammatory alterations in the prefrontal cortex of Wistar rats with epilepsy caused by lithium chloride and pilocarpine. Twenty-four male Wistar rats were randomly allocated into four groups: control, lithium-pilocarpine (LP), LP treated with Aframomum melegueta (400 mg/kg), and LP treated with carbamazepine (100 mg/kg). Seizures were elicited with the administration of lithium chloride, succeeded by pilocarpine. Behavioural evaluations were performed via the open field and Y-maze assessments. Prefrontal cortical tissues were examined for neurotransmitters (GABA and glutamate), oxidative stress indicators (malondialdehyde and superoxide dismutase), and the inflammatory cytokine (IL-6). Histological and immunohistochemical assessments were conducted utilising haematoxylin and eosin, Cresyl fast violet, Luxol fast blue, and GFAP staining techniques. Lithium-pilocarpine induction resulted in considerable behavioural abnormalities, an imbalance of excitatory and inhibitory neurotransmitters, heightened lipid peroxidation, diminished antioxidant activity, raised IL-6 levels, and pronounced neuronal degeneration, demyelination, and astrogliosis in the prefrontal cortex. Treatment with Aframomum melegueta markedly improved behavioural deficits, decreased glutamate and IL-6 concentrations, bolstered antioxidant defences, maintained neuronal and myelin integrity, and mitigated astrocytic activation, exhibiting results akin to carbamazepine. Aframomum melegueta demonstrates considerable neuroprotective properties against lithium-pilocarpine-induced damage in the prefrontal cortex, presumably via antioxidant, anti-inflammatory, and neuromodulatory pathways. The results endorse its potential as an adjunctive treatment agent in the management of epilepsy.

Introduction The present study evaluated oxidative stress indicators in plasma of beef calves supplemented with a rumen-protected methionine (L0 = receiving ration top-dressed with a ground corn carrier, L1 = receiving ration top-dressed with 10.0 g of rumen-protected methionine supplement in a ground corn carrier, L2 = receiving ration top-dressed with 20.0 g of rumen-protected methionine supplement in a ground corn carrier) and administered lipopolysaccharide (LPS). An additional objective evaluated the effect of LPS on plasma metabolites. Methods Following an initial feeding period (40 d), steers (n = 32; 379 kg ± 30.7) were intravenously administered LPS (0.25 μg/kg BW). Blood was collected via jugular catheter at -2, 0, 2, 4, 6, 8, 10, 12, 18, 24, 36, and 48 h relative to LPS administration (0 h). Plasma was analyzed for amino acid (AA) concentrations, ferric-reducing antioxidant power (FRAP), thiobarbituric reactive substances (TBARS), and reactive oxygen species (ROS). Metabolomic analysis occurred for control cattle at -2, 2, and 8 h. Results and discussion Plasma AA asparginine and methionine were increased with supplementation ( P < 0.01). The greatest FRAP values were observed at -2, 0, 2, 36, and 48 h ( P < 0.001). At 6 and 8 h, FRAP decreased to their lowest values ( P < 0.001). Amount of TBARS increased at 2 h but declined at 4h ( P < 0.001). A treatment × time interaction occurred for ROS ( P < 0.001). At 2 h, ROS was greatest in L0 cattle, least in L2, and intermediate in L1 but declined at 4 h in all treatments ( P < 0.001). Values peaked at 6 h for L1 and L2 cattle, followed by a decline at 8 h ( P < 0.001). Values for L0 cattle were similar from 4 to 6 h ( P = 0.371) but increased at 8 h ( P < 0.001). Finally, L0 plasma metabolites present at -2 h segregated from those present at 2 and 8 h ( P < 0.05). Differences were primarily driven by taurocholic acid, LysoPE, butyric acid, acitretin, and tauromuricholic acid. These data demonstrate that LPS may alter oxidative stress indicators and plasma metabolites. However, methionine supplementation may mitigate oxidative stress.

Background Estrogen plays a vital role in maintaining metabolic balance, and its decline due to menopause or ovariectomy (OVX) is closely linked to obesity, dyslipidemia, oxidative stress, and chronic inflammation. Black raspberry ( Rubus occidentalis , BR), a rich source of anthocyanins and phenolic acids, has demonstrated potent antioxidant and anti-inflammatory activities that may help counteract these adverse effects. However, its precise metabolic effects under estrogen-deficient conditions remain unclear. Objective This study aimed to investigate the effects of BR supplementation on lipid metabolism, oxidative stress, and inflammatory responses in an OVX rat model, with a focus on key signaling pathways in the liver, aorta, and adipose tissues. Methods OVX rats were fed diets supplemented with BR. Metabolic and inflammatory markers were measured in serum and relevant tissues. Key indicators of lipid metabolism, oxidative stress, and signaling pathway activity were assessed to determine the systemic impact of BR bioactives. Results BR supplementation improved lipid profiles, reduced oxidative stress markers, and suppressed pro-inflammatory mediators in the liver, aorta, and adipose tissues of OVX rats. Additionally, BR modulated signaling pathways associated with metabolic regulation and inflammation. Conclusions BR intake may mitigate estrogen deficiency-related metabolic disturbances by improving lipid metabolism, reducing oxidative stress, and modulating inflammatory responses, supporting its potential as a dietary strategy to promote metabolic health in postmenopausal conditions.