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Showing 3 results for Moosavi

Seyed Morteza Moosavi, Omid Pouresmaeil, Hengameh Zandi, Sahar Emadi, Fatemeh Akhavan, Alireza Torki, Akram Astani,
Volume 9, Issue 2 (Vol.9 No.2 Jul 2020)
Abstract

Background: Due to extensive damage to the skin, burn victims may acquire life-threatening infections. Though the skin primarily protects against microbial invasions, a large number of bacteria, fungi, and viruses can be isolated from burn patients, specifically Pseudomonas aeruginosa, a gram-negative bacterium with both intrinsic and acquired antibiotic resistance (AR) properties. nalB mutations can be found on the mexR in the P. aeruginosa chromosome. This mutation can induce overexpression of the mexAB-oprMoperon, and affect the MexAB-OprM efflux pump, which removes antimicrobial agents from the bacterial cell. Identifying nalB mutants can be useful for monitoring factors affecting AR.

Methods: In this study, 70 P. aeruginosa isolates identified from burn patients and antibacterial sensitivity was evaluated using the Kirby-Bauer method. We also investigated nalB mutations in samples using molecular methods including Polymerase reaction chain (PCR) and Sequencing.

Results: We identified nalB mutations in 16 isolates. We also found that the increasing effect of nalB mutants induces hyper production activity of MexAB-OprM resulting in AR. Overall, these findings compliment the findings of previous reports.

Conclusions: According to the resistance patterns of the samples, both Amikacin and Ciprofloxacin showed the highest resistance (%). Further, the relationship between Ciprofloxacin resistance and nalB mutations was statistically significant (p= 0.016). The results confirm that the increasing effect of nalB mutants on hyper production activity of MexAB-OprM leads to AR.

Mahdieh Sadat Badiee, Ali Vadizadeh, Maryam Salehcheh, Mehrnoosh Moosavi, Maryam Shirani, Fereshtesadat Fakhredini, Mohammad Javad Khodayar,
Volume 13, Issue 2 (Vol.13 No.2 Jul 2024)
Abstract

Background: The study focuses on evaluating the combined effects of quercetin (QCT) and catechin (CAT), both plant-based antioxidants, on alloxan-induced liver toxicity and diabetes in leptin-deficient (Lepob/ob) mice. Diabetes is a metabolic disorder characterized by high blood glucose levels due to inadequate insulin secretion or insulin resistance.

Methods: Thirty mice were divided into five groups of 6, including: normal control, diabetic control, diabetic mice treated with 150 mg/kg CAT, diabetic mice treated with 150 mg/kg QCT, and diabetic mice treated with 150 mg/kg CAT, and 150 mg/kg QCT for seven days. Mice were anesthetized after overnight fasting on the 8th day, and the blood sample was collected and the levels of antioxidants and pro-inflammatory factors in serum, and the expression of ADP-ribose polymerase (PARP) protein were measured, and histological studies were performed.

Results: The results showed that diabetic mice receiving QCT and CAT showed lower liver enzymes, fasting blood sugar (FBS), blood urea nitrogen (BUN), creatinine (Cr), cholesterol, triglyceride, low-density lipoprotein (LDL), TNF-α, and thiobarbituric acid reactive substances (TBARS) levels and increased high-density lipoprotein (HDL), total thiol, catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels in the liver compared to the ALLO group alone (P<0.001). The level of PARP protein significantly declined in the ALLO group compared to the control group.

Conclusion: The findings of this study demonstrated that QCT, and CAT are reasonably effective in preventing hepatotoxicity and diabetes in mice.
 

Mojgan Naghitorabi, Hadis Shayeganfar, Mohammad Javad Khodayar, Shahrzad Molavinia, Mehrnoosh Moosavi, Layasadat Khorsandi, Maryam Salehcheh,
Volume 14, Issue 1 (Vol.14 No.1 Apr 2025)
Abstract

Background: Paraquat (PQ) is a commonly used herbicide known for its high toxicity. Despite its hazardous nature, there are currently no effective treatments for PQ poisoning. This study aimed to evaluate the effects of Rosmarinic acid (RA), a phenolic compound, on PQ-induced lung injury in mice.

Methods: Mice were divided into ten groups for two experimental periods, 6- and 24-day periods (five groups each). The first group received normal saline daily, as the control group. Animals in the second group received a single intraperitoneal (i.p.) dose of PQ (25 mg/kg) on day 3. Groups three and four received RA (50 and 100 mg/kg, respectively) orally for 6 or 24 days. Group five received 100 mg/kg of RA daily. Animals were sacrificed 24 h after the last treatment, and lung samples were collected to determine histopathological changes and expression of TLR9, IL-1β, and TNF-α genes using RT-PCR.

Results: Hematoxylin and eosin staining revealed a significant reduction in lung injury following RA treatment. RA notably reduced inflammatory cell infiltration and lung tissue congestion. Furthermore, inflammatory responses triggered by PQ were suppressed after RA treatment, as demonstrated by the downregulation of IL-1β, TNF-α, and TLR9 levels.

Conclusion: These findings suggest the therapeutic potential of RA for mitigating PQ-induced lung damage and inflammation.



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