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

Abstract Background Cisplatin (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 p...

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Main Authors: Tayyaba Afsar, Suhail Razak, Ali Almajwal, Muhammad Rashid Khan
Format: Article
Language:English
Published: BMC 2018-02-01
Series:BMC Complementary and Alternative Medicine
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12906-018-2113-0
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spelling doaj-0b842ffbf7734ef7a5c97aeda71179aa2020-11-25T03:50:05ZengBMCBMC Complementary and Alternative Medicine1472-68822018-02-0118111310.1186/s12906-018-2113-0Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissueTayyaba Afsar0Suhail Razak1Ali Almajwal2Muhammad Rashid Khan3Department of Biochemistry, Faculty of Biological Sciences, Quaid-i-Azam UniversityDepartment of Animal Sciences, Faculty of Biological Sciences, Quaid-i-Azam UniversityDepartment of Community Health Sciences, College of Applied Medical Sciences, King Saud UniversityDepartment of Biochemistry, Faculty of Biological Sciences, Quaid-i-Azam UniversityAbstract Background Cisplatin (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. Methods Rats 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. Results CP 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. Conclusion These 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.http://link.springer.com/article/10.1186/s12906-018-2113-0DNA fragmentationPulmonary toxicityOxidative stress markersHistopathological alterations
collection DOAJ
language English
format Article
sources DOAJ
author Tayyaba Afsar
Suhail Razak
Ali Almajwal
Muhammad Rashid Khan
spellingShingle Tayyaba Afsar
Suhail Razak
Ali Almajwal
Muhammad Rashid Khan
Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue
BMC Complementary and Alternative Medicine
DNA fragmentation
Pulmonary toxicity
Oxidative stress markers
Histopathological alterations
author_facet Tayyaba Afsar
Suhail Razak
Ali Almajwal
Muhammad Rashid Khan
author_sort Tayyaba Afsar
title Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue
title_short Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue
title_full Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue
title_fullStr Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue
title_full_unstemmed Acacia hydaspica R. Parker ameliorates cisplatin induced oxidative stress, DNA damage and morphological alterations in rat pulmonary tissue
title_sort acacia hydaspica r. parker ameliorates cisplatin induced oxidative stress, dna damage and morphological alterations in rat pulmonary tissue
publisher BMC
series BMC Complementary and Alternative Medicine
issn 1472-6882
publishDate 2018-02-01
description Abstract Background Cisplatin (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. Methods Rats 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. Results CP 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. Conclusion These 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.
topic DNA fragmentation
Pulmonary toxicity
Oxidative stress markers
Histopathological alterations
url http://link.springer.com/article/10.1186/s12906-018-2113-0
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