Curcumin alone and in combination with augmentin protects against pulmonaryinflammation and acute lung injury generated during Klebsiella pneumoniae B5055-induced lung infection in BALB/c mice

Bansal, Shruti; Chhibber, Sanjay

doi:10.1099/jmm.0.016873-0

Cited by 63 publications

(53 citation statements)

References 41 publications

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“…These parmeters were significantly increased in the lung tissue of Klebsiella pneumoniae induced group as compared with control group. Similar results were reported by other researcher [19]. The increased activity of myloperoxidase enzyme is indicator of neutophil infiltration and its levels correlated with neutrophil numbers on all days of infection.…”

Section: Discussionsupporting

confidence: 91%

Comparative Study of CSE 1034 and Ceftriaxone in Pneumonia Induced Rat

Dwivedi¹

2012

Clin Exp Pharmacol

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Pneumonia caused by Klebsiella pneumoniae is important due to its high morbidity and mortality. This infection causes acute inflammation in the lung is characterized by increased activity of neutrophils, generate oxy free radical and decreased the endogenous anti oxidant defense system. CSE1034 is a novel fixed dose combination drug of ceftriaxone plus sulbactam with VRP1034. The aim of this investigation was to compare the efficacy study of CSE1034 drug vs ceftriaxone alone in pneumonia induced rat model. For pneumonia infection in animal model, doses were standardized at concentration 10 2 to 10 6 CFU/ml of Klebsiella pneumoniae.Total thirty two male rats (150 ± 5 g) were randomely selected and divided into four groups of eight animals each. Group I was normal saline treated; group II was pneumonia infected; group III was infected plus ceftriaxone treated and group IV was infected plus CSE1034 treated. Pneumonia infection was induced in all group except group I via intranasal instillation, at concentration (log 10 6 CFU/ml) for 15 days. Infection was confirmed by raised body temperature, bacterial count, cell count and cytokine (TNF-α, IL-6) parameters in blood. After conformation of infection, CSE1034 and ceftriaxone drugs treatment were stared for 15 days. At the end experiment, blood and lung tissue were collected and measured the biochemical and enzymatic parameters in all group.The finding showed that a significant decrease lactate dehydrogenase activity, malonaldialdehyde, total protein, albumin, nitrate, tumor necrosis factor-α, interlukin-6 levels and bacterial count along with increase reduced glutathione level in lung homogenate of CSE1034 treated group as compared to pneumonia induced and ceftriaxone treated groups. These findings suggested that CSE1034 is effective than ceftriaxone which reduced bacterial count and enhanced endogenous antioxidant status along with reduces, inflammatory response during pneumonia infection.

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Section: Discussionsupporting

confidence: 91%

Comparative Study of CSE 1034 and Ceftriaxone in Pneumonia Induced Rat

Dwivedi¹

2012

Clin Exp Pharmacol

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“…De et al have also elucidated antimicrobial activity of curcumin against helicobacter pylori (28). According to Bansal et al, research, curcumin was able to inhibit nosocomial infections caused by Klebsiella pneumonia, an opportunistic pathogen (31). These studies have been shown antimicrobial effect of curcumin while our study has displayed a higher potency of curcuminloaded chitosan-TPP nanoparticles rather than the individual curcumin.…”

Section: Discussioncontrasting

confidence: 42%

Curcumin-loaded Chitosan Tripolyphosphate Nanoparticles as a safe,natural and effective antibiotic inhibits the infection of Staphylococcusaureus and Pseudomonas aeruginosa in vivo

Jahromi¹,

Al-Musawi²,

Pirestani³

et al. 2014

Iran J Biotech

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“…• Significantly decreased the production of TNF-a in a mouse model of acute inflammation (Bansal and Chhibber, 2010).…”

Section: Figurementioning

confidence: 99%

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

339

239

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TNFs are major mediators of inflammation and inflammation-related diseases, hence, the United States Food and Drug Administration (FDA) has approved the use of blockers of the cytokine, TNF-a, for the treatment of osteoarthritis, inflammatory bowel disease, psoriasis and ankylosis. These drugs include the chimeric TNF antibody (infliximab), humanized TNF-a antibody (Humira) and soluble TNF receptor-II (Enbrel) and are associated with a total cumulative market value of more than $20 billion a year. As well as being expensive ($15 000-20 000 per person per year), these drugs have to be injected and have enough adverse effects to be given a black label warning by the FDA. In the current report, we describe an alternative, curcumin (diferuloylmethane), a component of turmeric (Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-a action and production in in vitro models, in animal models and in humans. In addition, we provide evidence for curcumin's activities against all of the diseases for which TNF blockers are currently being used. Mechanisms by which curcumin inhibits the production and the cell signalling pathways activated by this cytokine are also discussed. With health-care costs and safety being major issues today, this golden spice may help provide the solution. LINKED ARTICLESThis article is part of a themed section on Emerging Therapeutic Aspects in Oncology. To view the other articles in this section visit http://dx

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Curcumin alone and in combination with augmentin protects against pulmonaryinflammation and acute lung injury generated during Klebsiella pneumoniae B5055-induced lung infection in BALB/c mice

Cited by 63 publications

References 41 publications

Comparative Study of CSE 1034 and Ceftriaxone in Pneumonia Induced Rat

Comparative Study of CSE 1034 and Ceftriaxone in Pneumonia Induced Rat

Curcumin-loaded Chitosan Tripolyphosphate Nanoparticles as a safe,natural and effective antibiotic inhibits the infection of Staphylococcusaureus and Pseudomonas aeruginosa in vivo

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

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