Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of <i>Chloranthus serratu</i>s

Sun, Shuping; Wang, Yang; Du, Yunyan; Sun, Qi; He, Lu; Zhu, Enze; Li, Jiarong

doi:10.1080/13880209.2020.1859552

Cited by 10 publications

(6 citation statements)

References 36 publications

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“…As the pathology of diabetic nephropathy is associated with the overproduction of early response pro-inflammatory cytokines ( He et al, 2022 ), we determined the inflammatory biomarkers ( Sun et al, 2020b ; Wang et al, 2020b ). STZ treatment induced a significant increase in the levels of IL-1β, IL-6, and TNF-α ( Figures 2A–C ) in rats exposed to Cd when compared to those of control rats.…”

Section: Resultsmentioning

confidence: 99%

Zn(II)–curcumin prevents cadmium-aggravated diabetic nephropathy by regulating gut microbiota and zinc homeostasis

Sun,

Mei,

Wang

et al. 2024

Front. Pharmacol.

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Background: Diabetic nephropathy (DN) is known as the most common complication of diabetes, resulting from a complex inheritance-environment interaction without effective clinical treatments. Herein, we revealed the protective effects and mechanisms of Zn(II)-curcumin, a curcumin derivative, against streptozotocin-induced DN in rats in the presence or absence of cadmium exposure.Methods: The present study focused on investigating the therapy of Zn(II)-curcumin against cadmium-aggravated DN by regulating gut microbiota, metabolism, inflammation and zinc homeostasis based on pathological changes, TLR4/NF-κB signaling pathway, inductively coupled plasma-mass spectrometry (ICP-MS), 16S rRNA gene sequencing and gas chromatography-mass spectrometer (GC-MS).Results: We found Zn(II)-curcumin significantly mitigated the cadmium-aggravated phenotypes of diabetic nephropathy, as indicated by the remission of renal dysfunction, pathological changes, inflammation and zinc dyshomeostasis in streptozotocin-treated rats exposed to cadmium. Administration of Zn(II)-curcumin significantly alleviated the dysbiosis of gut microbiota and the changes of serum metabolite profiles in rats treated with streptozotocin in combination with cadmium. Notably, fecal microbial transplantation identified the ability of Zn(II)-curcumin to regulate renal function, inflammation and zinc homeostasis was partly dependent on the gut microbiota.Conclusion: These findings revealed that Zn(II)-curcumin alleviated cadmium-aggravated diabetic nephropathy by reshaping the gut microbiota and zinc homeostasis, which provided unique insights into the mechanisms of the treatment and prevention of diabetic nephropathy.

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Section: Resultsmentioning

confidence: 99%

Zn(II)–curcumin prevents cadmium-aggravated diabetic nephropathy by regulating gut microbiota and zinc homeostasis

Sun,

Mei,

Wang

et al. 2024

Front. Pharmacol.

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“…The dysregulation of hepatic glucose metabolism probably results from the oxidative damage to enzymes that are related to the glycolysis, tricarboxylic acid cycle and ATP biosynthesis ( Jha and Mazumder, 2019 ). Therefore, targeting oxidative stress to improve the metabolism of glucose in liver has been suggested as a strategy for the treatment of hepatotoxicity, diabetes and its complications ( Sun et al, 2020b ). For example, dapagliflozin protects hyperglycemia-induced cardiomyocytes damage through inhibiting NADPH oxidase-mediated oxidative stress ( Xing et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

N-p-coumaroyloctopamine ameliorates hepatic glucose metabolism and oxidative stress involved in a PI3K/AKT/GSK3β pathway

Huang,

Zhang,

et al. 2024

Front. Pharmacol.

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Type 2 diabetes mellitus is regarded as a chronic metabolic disease characterized by hyperglycemia. Long-term hyperglycemia may result in oxidative stress, damage pancreatic β-cell function and induce insulin resistance. Herein we explored the anti-hypoglycemic effects and mechanisms of action of N-p-coumaroyloctopamine (N-p-CO) in vitro and in vivo. N-p-CO exhibited high antioxidant activity, as indicated by the increased activity of SOD, GSH and GSH-Px in HL-7702 cells induced by both high glucose (HG) and palmitic acid (PA). N-p-CO treatment significantly augmented glucose uptake and glycogen synthesis in HG/PA-treated HL-7702 cells. Moreover, administration of N-p-CO in diabetic mice induced by both high-fat diet (HFD) and streptozotocin (STZ) not only significantly increased the antioxidant levels of GSH-PX, SOD and GSH, but also dramatically alleviated hyperglycemia and hepatic glucose metabolism in a dose-dependent manner. More importantly, N-p-CO upregulated the expressions of PI3K, AKT and GSK3β proteins in both HG/PA-induced HL-7702 cells and HFD/STZ-induced mice. These findings clearly suggest that N-p-CO exerts anti-hypoglycemic and anti-oxidant effects, most probably via the regulation of a PI3K/AKT/GSK3β signaling pathway. Thus, N-p-CO may have high potentials as a new candidate for the prevention and treatment of diabetes.

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“…Complement mediators, particularly C3a, can activate neutrophils, mast cells, monocytes/macrophages, T cells, B cells, etc. [ 107 – 109 ]. The complement system is activated predominantly via three pathways—classical, lectin, and alternative—which converge in C3 activation.…”

Section: Discussionmentioning

confidence: 99%

The effect of modified Qiyuan paste on mice with low immunity and sleep deprivation by regulating GABA nerve and immune system

Rong,

Jia,

Lin

et al. 2024

Chin Med

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Background Low immunity and sleep disorders are prevalent suboptimal health conditions in contemporary populations, which render them susceptible to the infiltration of pathogenic factors. LJC, which has a long history in traditional Chinese medicine for nourishing the Yin and blood and calming the mind, is obtained by modifying Qiyuan paste. Dendrobium officinale Kimura et Migo has been shown to improve the immune function in sleep-deprived mice. In this study, based on the traditional Chinese medicine theory, LJC was prepared by adding D. officinale Kimura et Migo to Qiyuan paste decoction. Methods Indicators of Yin deficiency syndrome, such as back temperature and grip strength, were measured in each group of mice; furthermore, behavioral tests and pentobarbital sodium-induced sleep tests were performed. An automatic biochemical analyzer, enzyme-linked immunosorbent assay kit, and other methods were used to determine routine blood parameters, serum immunoglobulin (IgG, IgA, and IgM), cont (C3, C4), acid phosphatase (ACP) and lactate dehydrogenase (LDH) levels in the spleen, serum hemolysin, and delayed-type hypersensitivity (DTH) levels. In addition, serum levels of γ-aminobutyric acid (GABA) and glutamate (Glu) were detected using high-performance liquid chromatography (HPLC). Hematoxylin–eosin staining and Nissl staining were used to assess the histological alterations in the hypothalamus tissue. Western blot and immunohistochemistry were used to detect the expressions of the GABA pathway proteins GABRA1, GAD, GAT1, and GABAT1 and those of CD4+ and CD8+ proteins in the thymus and spleen tissues. Results The findings indicated that LJC prolonged the sleep duration, improved the pathological changes in the hippocampus, effectively upregulated the GABA content in the serum of mice, downregulated the Glu content and Glu/GABA ratio, enhanced the expressions of GABRA1, GAT1, and GAD, and decreased the expression of GABAT1 to assuage sleep disorders. Importantly, LJC alleviated the damage to the thymus and spleen tissues in the model mice and enhanced the activities of ACP and LDH in the spleen of the immunocompromised mice. Moreover, serum hemolysin levels and serum IgG, IgA, and IgM levels increased after LJC administration, which manifested as increased CD4+ content, decreased CD8+ content, and enhanced DTH response. In addition, LJC significantly increased the levels of complement C3 and C4, increased the number of white blood cells and lymphocytes, and decreased the percentage of neutrophils in the blood. Conclusions LJC can lead to improvements in immunocompromised mice models with insufficient sleep. The underlying mechanism may involve regulation of the GABA/Glu content and the expression levels of GABA metabolism pathway-related proteins in the brain of mice, enhancing their specific and nonspecific immune functions. Graphical Abstract

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Oxidative stress-mediated hepatotoxicity in rats induced by ethanol extracts of different parts of Chloranthus serratus

Cited by 10 publications

References 36 publications

Zn(II)–curcumin prevents cadmium-aggravated diabetic nephropathy by regulating gut microbiota and zinc homeostasis

Zn(II)–curcumin prevents cadmium-aggravated diabetic nephropathy by regulating gut microbiota and zinc homeostasis

N-p-coumaroyloctopamine ameliorates hepatic glucose metabolism and oxidative stress involved in a PI3K/AKT/GSK3β pathway

The effect of modified Qiyuan paste on mice with low immunity and sleep deprivation by regulating GABA nerve and immune system

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