Oxidative Medicine and Cellular Longevity最新文献

[This corrects the article DOI: 10.1155/2015/358396.].

[This corrects the article DOI: 10.1155/2022/6371048.].

Regular hookah smoking (Reg-HS) has become a major global public health issue, linked to significant health risks, including kidney damage. A less frequent pattern of use, known as occasional hookah smoking (Occ-HS), is also common; however, there has been little progress in understanding the direct impact of Occ-HS on kidneys. To investigate how varying frequencies of HS inhalation affect the kidney, we exposed mice to nose-only HS under two regimens, occasional (30 min once weekly) and regular (30 min five times per week) for a duration of 6 months. This study explored the impact on renal damage, inflammatory responses, oxidative stress levels, genotoxicity, and mitochondrial activity as well as the possible modulation of MAPK signaling pathway. Both Occ-HS and Reg-HS led to a marked elevations in plasma levels of urea and creatinine (p < 0.05-p < 0.0001). Additionally, concentrations of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) were significantly increased in both groups (p < 0.01-p < 0.0001). Notably, only the Reg-HS regimen induced a substantial rise in plasma levels of indoxyl sulfate, cystatin C, and adiponectin (p < 0.01-p < 0.0001). Similarly, relative to the control group, mice subjected to Reg-HS exposure exhibited significantly elevated levels of proinflammatory cytokines, tumor necrosis factor-α, and interleukin-6 (p < 0.0001). Exposure to either Occ-HS or Reg-HS caused significant increase in interleukin-1β (p < 0.05, p < 0.0001), thiobarbituric acid reactive substances (TBARS; p < 0.05, p < 0.0001) compared with air-exposed mice. Our findings revealed that Occ-HS inhalation triggered only a decrease in superoxide dismutase (SOD) activity (p < 0.001). On the other hand, nitric oxide (NO; p < 0.001), SOD (p < 0.0001), and Glutathione (GSH; p < 0.0001) levels were significantly decreased in Reg-HS group. Furthermore, DNA damage marker, 8-Hydroxy-2^'-deoxyguanosine was significantly augmented in both regimens (p < 0.0001). Exposure to both regimens resulted in significant elevation in mitochondrial complexes I, II and III, and IV (p < 0.0001). Increased expression of activation of mitogen-activated protein kinases (MAPKs) was observed exclusively in the Reg-HS group, as evidenced by increased levels of p-JNK, p-p38, and p-ERK (p < 0.001-p < 0.0001). In conclusion, our study is the first to demonstrate that despite the significant differences in the amount of smoke inhaled, both Occ-HS or Reg-HS inhalation deteriorate kidney function and induce oxidative damage, inflammatory response, DNA injury, and mitochondrial impairment with modulation of the MAPK signaling. These findings highlight the importance of further research into the public health risks associated with occasional hookah smoking.

[This retracts the article DOI: 10.1155/2019/2432416.].

Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Emerging evidence suggests a rising incidence of CRC in younger adults, emphasizing the urgent need for innovative therapeutic strategies. The increasing attention on circular economy approaches has heightened interest in discovering natural compounds derived from recycled agri-food waste. These compounds are particularly promising due to their large array of bioactive functional components. In this study, we investigated the efficacy of a green compost derived from coffee wastes, known as humic substance (HS), in reducing CRC cell viability. Chemical characterization of HS from composted coffee waste (HS-COF) using ¹³C Cross-Polarization Magic-Angle Spinning Nuclear Magnetic Resonance (CPMAS NMR) spectroscopy and offline pyrolysis Tetramethylammonium Hydroxide-Gas Cromatography Mass-Spectrometry (TMAH-GC-MS) revealed an abundance of phenolic compounds derived from lignin residues. Specifically, chlorogenic acid (ClA) was identified as the major component and primary agent responsible for the biological effects of HS-COF. Our in vitro results demonstrated that HS-COF selectively inhibits HT-29 cell viability, migration, and proliferation by inducing programed cell death through the activation of the tumor necrosis factor-α (TNF-α) signaling pathway and disruption of calcium homeostasis. Additionally, HS-COF exhibited a significant antioxidant activity, indicating its potential to combine a cytotoxic profile with a safety profile, thereby minimizing adverse effects on healthy cells. In conclusion, this study proposes HS-COF as a valuable adjuvant in CRC therapy, paving the way for its application in the pharmaceutical industry.

Background and purpose: Liver fibrosis poses a major global health burden, contributing substantially to morbidity and mortality worldwide. This study aims to assess the potential novel mechanisms behind the anti-fibrotic effects of sotagliflozin (Sota) in thioacetamide (TAA)-induced liver fibrosis in rats.

Experimental approach: To induce liver fibrosis in rats, 100 mg/kg of TAA was injected intraperitoneally triweekly for 6 weeks. Treated groups were orally administered sotagliflozin (10 and 20 mg/kg) for 4 weeks, concurrent with TAA injections.

Key results: Alongside the histological alterations, the elevation of liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST), lipid profiles total cholesterol (TC) and triglycerides (TAG), cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), apoptotic markers (caspase-3 and Bcl2 associated X protein [Bax] BAX), phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT), and the lipid peroxidation marker malondialdehyde (MDA) indicated liver dysfunction induced by TAA. Furthermore, indicators of liver fibrosis encompassed reduced levels of albumin, antioxidants; glutathione (GSH), superoxide dismutase (SOD), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2), antiapoptotic protein B-cell lymphoma-2 (BCL2), sirtuin-1 (SIRT1) expression, and histopathological alterations.

Conclusion and implications: This study demonstrated that daily oral treatment with sotagliflozin markedly upregulated antioxidant markers such as SIRT1 and Nrf2, attenuated TNF-α, and reduced apoptotic and fibrogenic markers, thereby protecting against TAA-induced liver fibrosis. This may have occurred through the augmentation of SIRT1/Nrf2 expression, the inhibition of PI3K/AKT, resulting in the suppression of apoptosis and inflammation.

[This retracts the article DOI: 10.1155/2012/486190.].

[This retracts the article DOI: 10.1155/2020/3035624.].

[This corrects the article DOI: 10.1155/2021/2999296.].

[This corrects the article DOI: 10.1155/2018/1874985.].