Methanolic bark extract of <i>Acacia catechu</i> ameliorates benzo(a)pyrene induced lung toxicity by abrogation of oxidative stress, inflammation, and apoptosis in mice

Shahid, Ayaz; Rashid, Asif; Ali, Nemat; Hasan, Syed Kazim; Barnwal, Preeti; Afzal, Shekh Mohammad; Vafa, Abul; Sultana, Sarwat

doi:10.1002/tox.22382

Cited by 32 publications

(31 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results were in line with the study of Ayaz and coworkers indicating that pretreatment with methanolic bark extract of Acacia catechu (400 mg/kg body weight) significantly ameliorates benzo(a)pyrene induced increased toxicity markers and activities of detoxifying enzymes along with the levels of glutathione content. The underlying mechanism is the attenuated expression of apoptotic and inflammatory markers in the lungs [ 33 ]. Polyphenolic in A. hydaspica AHE fraction might be responsible for the protective effect via diminishing oxidative stress and increasing the antioxidant enzyme status.…”

Section: Discussionmentioning

confidence: 99%

“…Pretreatment with MEBA at two different doses (200 and 400 mg/kg body weight) significantly ameliorates B(a)P-induced increased toxicity markers and activities of detoxifying enzymes along with the levels of glutathione content. It also significantly attenuated expression of apoptotic and inflammatory markers in the lungs and attenuated destruction of alveolar architecture and necrosis of the alveolar epithelium of the lungs [ 33 ]. Acacia honey ameliorated sodium arsenide persuaded oxidative trauma in the cardiac, pulmonary, and renal tissues of rats due to its antioxidant potential and polyphenol components [ 34 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue

Afsar

Razak

Almajwal

et al. 2018

BMC Complement Altern Med

View full text Add to dashboard Cite

BackgroundCisplatin (CP) drug is platinum compounds used for the treatment of various human malignancies. However, adverse outcomes related to CP restrict its usage. Acacia hydaspica is a natural shrub with various pharmacological properties. The current investigation aimed to assess the protective potential of A. hydaspica polyphenol rich ethyl acetate extract (AHE) against cisplatin (CP) induced pulmonary toxicity.MethodsRats were divided into six groups. Group 1 served as control (saline); Group 2 (drug control) recieved single dose of CP (7.5 mg/kg i.p.) on 1st day; Group 3 (extract control) (400 mg/kg bw, p.o.) received AHE for one week; Group 4 (Post-treated) and Group 5 (pretreated) received AHE (400 mg/kg bw/day, p.o) for 7 days after and before CP (7.5 mg/kg b.w., i.p.) respectively; Group 6 (Standard control) received silymarin (100 mg/kg b.w/7 days) before CP. At the end of dosing rats were sacrificed and pulmonary tissue samples were processed for the evaluation of antioxidant enzymes, oxidative stress markers, genotoxicity and histopathological alterations.ResultsCP caused body weights loss and increase pulmonary tissue weight. The CP significantly increases oxidative stress markers and decreases tissue antioxidant enzyme levels. Furthermore, CP induced deleterious changes in the microanatomy of pulmonary tissue by rupturing the alveolar septa, thickening of alveolar walls, and injuring the cells with subsequent collapse of blood vessels. AHE pretreatment returned MDA, NO, H2O2 production and improved tissue antioxidant enzyme levels to near normalcy. The histological observations evidenced that AHE effectively rescues the lungs from CP-mediated oxidative damage. CP induction in rats also caused DNA fragmentation which was restored by AHE treatment. Our results suggest that pretreatment more significantly improve CP induced deleterious effects compared with post treatment indicating protective effect. Potency of AHE pretreatment is similar to silymarin.ConclusionThese findings demonstrated that A. hydaspica AHE extract might serve as potential adjuvant that prevents CP persuaded pulmonary toxicity due to its intrinsic antioxidant potential and polyphenolic constituents.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue

Afsar

Razak

Almajwal

et al. 2018

BMC Complement Altern Med

View full text Add to dashboard Cite

show abstract

“…However, persistent and excessive autophagy leads to cell death (Swart et al, 2016). Previous studies unraveled that BaP promotes the release of pro-inflammatory cytokines and increases the protein expression of iNOS in mice colon (Ajayi et al, 2016), lungs (Shahid et al, 2016;Shahid et al, 2017), airway (Yangisawa et al, 2016), and intestine (Ribiere et al, 2016) and zebrafish embryos (Duan et al, 2016). That is to say, BaP triggers inflammation.…”

Section: Introductionmentioning

confidence: 98%

Benzo[a]pyrene induces pyroptotic and autophagic death through inhibiting PI3K/Akt signaling pathway in HL-7702 human normal liver cells

Gao

Deng

et al. 2019

J. Toxicol. Sci.

View full text Add to dashboard Cite

-Benzo(α)pyrene (BaP) possesses a forceful hepatotoxicity, and is ubiquitous in foods and ambient air. Our previous study found that BaP induced pyroptotic and autophagic death in HL-7702 human liver cells; the relevant mechanisms, however, remain unknown. This work was therefore to unravel the effects of the PI3K/Akt signaling pathway on pyroptotic and autophagic death triggered by BaP. Cells were treated with or without LY294002 (PI3K/Akt inhibitor) and IGF-1 (PI3K/Akt activator) before BaP exposure, and the results showed that compared with the control, the protein expression of p-Akt was markedly decreased by BaP (p < 0.05). IGF-1 did not subvert this inhibitive effect of BaP, while LY294002 enhanced it. Furthermore, the protein expression of pyroptosis (Cleaved Caspase-1, NO, IL-1β, IL-18), as well as LDH and the relative electrical conductivity were significantly augmented by BaP. The levels of these indices were increased by LY294002 pretreatment, and decreased by IGF-1. Similarly, LY294002 enhanced BaP-induced increase in the key protein expression of autophagy (Beclin-1 and LC3II), while IGF-1 weakened it. Finally, the phosphorylation of FOXO4 was clearly (p < 0.01) inhibited by BaP, and LY294002 suppressed this inhibitive effect of BaP, while IGF-1 strengthened it. In conclusion, BaP was able to induce pyroptotic and autophagic death via blocking the PI3K/Akt signaling pathway in HL-7702 liver cells.

show abstract

“…To examine the in vivo anti-inflammatory effect of HJE compared with NHJE, a B(a)P-induced acute lung inflammation mouse model was employed [ 2 , 36 , 40 ]. B(a)P is the most common and toxic polycyclic aromatic hydrocarbon, an environmental pollutant, and reportedly the cause of health problems, such as redox imbalance, respiratory diseases, and cancer [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

In Vivo Anti-Inflammatory Potential of Viscozyme®-Treated Jujube Fruit

Kim

Jang

et al. 2020

Foods

View full text Add to dashboard Cite

The fruit of Ziziphus jujuba, commonly called jujube, has long been consumed for its health benefits. The aim of this study was to examine the protective effect of dietary supplementation of enzymatically hydrolyzed jujube against lung inflammation in mice. The macerated flesh of jujube was extracted with aqueous ethanol before and after Viscozyme treatment. The extract of enzyme-treated jujube, called herein hydrolyzed jujube extract (HJE), contained higher levels of quercetin, total phenolics, and flavonoids, and exhibited more effective radical-scavenging abilities in comparison to non-hydrolyzed jujube extract (NHJE). HJE treatment decreased production of inflammation-associated molecules, including nitric oxide and pro-inflammatory cytokines from activated Raw 264.7 or differentiated THP-1 cells. HJE treatment also reduced expression of nuclear factor-κB and its downstream proteins in A549 human lung epithelial cells. Moreover, oral supplementation of 1.5 g of HJE per kg of body weight (BW) attenuated histological lung damage, decreased plasma cytokines, and inhibited expression of inflammatory proteins and oxidative stress mediators in the lungs of mice exposed to benzo(a)pyrene at 50 mg/kg BW. Expression levels of antioxidant and cytoprotective factors, such as nuclear factor erythroid-derived 2-related factor 2 and heme oxygenase-1, were increased in lung and liver tissues from mice treated with HJE, compared to mice fed NHJE. These findings indicate that dietary HJE can reduce benzo(a)pyrene-induced lung inflammation by inhibiting cytokine release from macrophages and promoting antioxidant defenses in vivo.

show abstract

Methanolic bark extract of Acacia catechu ameliorates benzo(a)pyrene induced lung toxicity by abrogation of oxidative stress, inflammation, and apoptosis in mice

Cited by 32 publications

References 46 publications

Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue

Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue

Benzo[a]pyrene induces pyroptotic and autophagic death through inhibiting PI3K/Akt signaling pathway in HL-7702 human normal liver cells

In Vivo Anti-Inflammatory Potential of Viscozyme®-Treated Jujube Fruit

Contact Info

Product

Resources

About