Complexation of luteolin with lead (II): Spectroscopy characterization and theoretical researches

Wang, Qian; Zhao, Lingling; Zhao, Haoan; Li, Xinyan; Gao, Liguo; Ni, Cheng; Cao, Wei

doi:10.1016/j.jinorgbio.2019.01.007

Cited by 21 publications

(10 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study speculated that LUT may eliminate Pb through its effective chelating properties. 25 Accumulative evidences confirmed the development of oxidative stress in the brain tissue following Pb intoxication. 23,26 Brain is characterized by poor antioxidant capacity, enrich lipid content, and high oxygen consumption rate.…”

Section: Discussionmentioning

confidence: 94%

Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats

et al. 2020

View full text Add to dashboard Cite

Luteolin (LUT) is a glycosylated flavonoid compound that has multiple beneficial pharmacological and biological impacts. The current investigation was undertaken to evaluate the putative neuroprotective potency of LUT against neuronal damage induced by lead acetate (PbAc). Twenty-eight rats were placed into four equal groups. Group 1: served as the control group, group 2: rats were supplemented orally with LUT (50 mg kg−1), group 3: rats were intraperitoneally injected with PbAc (20 mg kg−1), and group 4: rats were pretreated with LUT before PbAc injection with the same doses. All animals were treated for 7 days. The exposure to PbAc increased the concentration of lead in the cortical tissue, neuronal lipid peroxidation, and nitric oxide (NO) production and decreased the antioxidant enzymes. Additionally, PbAc enhanced a neuroinflammatory response in the cortical tissue through increasing the pro-inflammatory cytokines secretion and inducible NO synthase expression. Moreover, cortical cell death was recorded following PbAc intoxication as evidenced by the enhancement of the proapoptotic and inhibiting the antiapoptotic markers. Interestingly, LUT supplementation reversed the cortical adverse reactions induced by PbAc. Taken together, these findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.

show abstract

Section: Discussionmentioning

confidence: 94%

Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Furthermore, the group exposed to dual treatment with LUT+PbAc exhibited a marked decline in hepatic Pb concentrations. A previous report speculated that luteolin may provide protection against Pb-induced health deficits through its promising chelating properties [40]. Flavonoids possess a metal-chelating ability and can bind with metals to form a metal-flavonoid complex.…”

Section: Discussionmentioning

confidence: 99%

Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities

et al. 2019

View full text Add to dashboard Cite

The abundant use of lead (Pb; toxic heavy metal) worldwide has increased occupational and ecosystem exposure, with subsequent negative health effects. The flavonoid luteolin (LUT) found in many natural foodstuffs possesses antioxidant and anti-inflammatory properties. Herein, we hypothesized that LUT could mitigate liver damage induced by exposure to lead acetate (PbAc). Male Wistar rats were allocated to four groups: control group received normal saline, LUT-treated group (50 mg/kg, oral, daily), PbAc-treated group (20 mg/kg, i.p., daily), and LUT+PbAc-treated group (received the aforementioned doses via the respective routes of administration); the rats were treated for 7 days. The results revealed that PbAc exposure significantly increased hepatic Pb residue and serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin value. Oxidative reactions were observed in the liver tissue following PbAc intoxication, characterized by the depletion and downregulation of antioxidant proteins (glutathione, glutathione reductase, glutathione peroxidase, superoxide dismutase, catalase, nuclear factor erythroid 2-related factor 2, and heme oxygenase-1), and an increase in oxidants (malondialdehyde and nitric oxide). Additionally, PbAc increased the release and expression of the pro-inflammatory cytokines (tumor necrosis factor alpha and interleukin-1 beta), inducible nitric oxide synthase, and nuclear factor kappa B. Moreover, PbAc enhanced hepatocyte loss by increasing the expression of pro-apoptotic proteins (Bax and caspase-3) and downregulating the anti-apoptotic protein (Bcl-2). The changes in the aforementioned parameters were further confirmed by noticeable histopathological lesions. LUT supplementation significantly reversed all of the tested parameters in comparison with the PbAc-exposed group. In conclusion, our findings describe the potential mechanisms involved in the alleviation of PbAc-induced liver injury by luteolin via its potent anti-inflammatory, antioxidant, and anti-apoptotic properties.

show abstract

“…Flavonoids are a group of polyphenolic compounds, with extensive pharmacologic properties (e.g., antioxidant, anti-inflammatory, hepatoprotective, anticarcinogenic) ( Choy et al., 2019 ; Wang S. W. et al., 2019 ). The functional oxo groups and hydroxyl groups of flavonoids play a key part in metal-chelating capacities ( Wang Q. et al., 2019 ). Lead-kaempferol- and lead-quercetin-chelating complexes possess strong antioxidant abilities in ferric reducing power assay and ABTS radical-scavenging systems ( Wang et al., 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Smilax glabra Roxb. Against Lead-Induced Renal Oxidative Stress, Inflammation and Apoptosis in Weaning Rats and HEK-293 Cells

Shi

Tian

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Lead (Pb) is an important environmental pollutant. Oxidative stress and the inflammatory response have been postulated as mechanisms involved in lead-induced renal damage. Smilax glabra Roxb. has been used for treatment of heavy-metal poisoning in China for 500 years. We investigated S. glabra flavonoids extract (SGF) could attenuate lead acetate-induced nephrotoxicity in weaning rats and human embryonic kidney (HEK)-293 cells, and investigated the possible mechanisms. Compared with Pb exposed group of weaning rats, SGF could significantly promote lead excretion in the blood and kidney, and increase the content of the renal-function indicators blood urea nitrogen, serum uric acid, and serum creatinine. SGF could improve the glomerular filtration rate (GFR) and histologic changes in the kidneys of weaning rats exposed to Pb. SGF could also reduce lead-induced cytotoxicity, improve DNA damage-induced apoptosis and cleaved caspase-3-mediated apoptosis in HEK-293 cells stimulated with Pb. SGF significantly increased the activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase and catalase, and decreased excessive release of reactive oxygen species (ROS) and malondialdehyde in the kidneys of the weaning rats and in HEK-293 cells. The antioxidant mechanism of SGF related to activation of the Kelch-like ECH-associated protein 1/nuclear-factor-E2-related factor 2/hemeoxygenase-1(Keap1/Nrf2/HO-1) pathway. SGF could inhibit secretion of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α induced by Pb in vivo and in vitro . The anti-inflammatory mechanism of SGF related to inhibition of ROS and pro-inflammatory cytokines triggered the nuclear factor-kappa B (NF-κB) pathway through blockade of inhibitors of I-κB degradation, phosphorylation of NF-κB p65, and nuclear translocation of p65. Our findings indicate that SGF could be a natural antioxidant and anti-inflammatory agent for treating lead-induced nephrotoxicity.

show abstract

Complexation of luteolin with lead (II): Spectroscopy characterization and theoretical researches

Cited by 21 publications

References 38 publications

Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats

Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats

Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities

Protective Effects of Smilax glabra Roxb. Against Lead-Induced Renal Oxidative Stress, Inflammation and Apoptosis in Weaning Rats and HEK-293 Cells

Contact Info

Product

Resources

About