Leptin concentrations are altered in favour of pro health after periodontal therapy. Leptin, a no... more Leptin concentrations are altered in favour of pro health after periodontal therapy. Leptin, a non-glycosylated peptide hormone, not only maintains fat stores, but is also an integral part of host defense repertoire. Leptin levels have been found to be altered in an array of inflammatory diseases including chronic periodontitis (CP), but the role of non-surgical periodontal therapy (NSPT) in altering the leptin concentrations in saliva and serum of CP patients is yet to be ascertained. The aim of the present study is to quantify leptin levels in CP patients having normal body mass index (BMI) pre-therapy as compared to periodontally healthy controls and to address whether successful NSPT alters leptin concentration in serum and saliva. Twenty-two saliva (modified draining method) and serum samples (by venipuncture) were collected from CP patients with normal BMI (n = 22), before and at 4 and 12 weeks after completion of NSPT, and periodontally healthy, age- and gender-matched controls (n = 22). Leptin levels were estimated using enzyme linked immunosorbent assay kits. At baseline, CP patients had significantly different periodontal clinical parameters and the leptin concentrations in saliva of CP patients were found to be significantly lower than periodontally healthy volunteers (4710.10 ± 1133.21 vs 8721.10 ± 1019.58 pg/ml) (p < 0.05), whereas in serum the leptin concentrations were significantly higher than healthy controls (10749 ± 2062.24 vs 8085.00 ± 2859.68 pg/ml). Significant improvement in periodontal parameters, serum and salivary leptin levels were observed in CP patients at 4 and 12 weeks post-therapy (p < 0.01). Altered concentrations of leptin in serum and saliva are observed in CP patients which can be restored in favor of health after periodontal therapy.
Background: The aim of this study is to investigate the impact of diabetes, a known risk factor f... more Background: The aim of this study is to investigate the impact of diabetes, a known risk factor for periodontitis, on activities of antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) as well as levels of free radical damage marker malondialdehyde (MDA) in blood and saliva of individuals with chronic periodontitis (CP).Methods: Sixty patients with CP (30 patients with type 2 diabetes mellitus [DMCP] and 30 systemically healthy patients [CP]) and 60 periodontally healthy individuals (30 patients with type 2 diabetes mellitus and 30 systemically healthy patients [PH]) were included in this study. After clinical measurements, blood and saliva samples were collected. SOD, GR, and CAT activities in red blood cell lysate and saliva and MDA levels in plasma and saliva samples were spectrophotometrically assayed. An analysis of variance test followed by a post hoc test was used to compare the intragroup and intergroup variances among the study grou...
Induction of tumor necrosis factor-α (TNF-α) in response to lead (Pb) exposure has been implicate... more Induction of tumor necrosis factor-α (TNF-α) in response to lead (Pb) exposure has been implicated in its immunotoxicity. However, the molecular mechanism by which Pb upregulates the level of TNF-α is wagely known. An attempt was therefore made to elucidate the mechanistic aspect of TNF-α induction, mainly focusing transcriptional and post transcriptional regulation via mitogen activated protein kinases (MAPKs) activation. We observed that exposure of Pb to human monocytic THP-1 cells resulted in significant enhanced production of TNF-α m-RNA and protein secretion. Moreover, the stability of TNF-α m-RNA was also increased as indicated by its half life. Notably, activation of ERK 1/2, p38 and JNK in Pb exposed THP-1 was also evident. Specific inhibitor of ERK1/2, PD 98059 caused significant inhibition in production and stability of TNF-α m-RNA. However, SB 203580 partially inhibited production and stability of TNF-α m-RNA. Interestingly, a combined exposure of these two inhibitors completely blocked modulation of TNF-α m-RNA. Data tends to suggest that expression and stability of TNF-α induction due to Pb exposure is mainly regulated through ERK. Briefly, these observations are useful in understanding some mechanistic aspects of proinflammatory and immunotoxicity of Pb, a globally acknowledged key environmental contaminant.
American Journal of Neuroprotection and Neuroregeneration, 2013
ABSTRACT The aim of the present study was to time coarse assessment of aluminum chloride induced ... more ABSTRACT The aim of the present study was to time coarse assessment of aluminum chloride induced macromolecular changes by in vivo magnetization transfer brain imaging and therapeutic efficacies of Bacopa monnieri (BM) have been investigated. In the present study, 100 mg/kg of AlCl3 daily was administered orally to rats and co-administered with BM (40 mg/kg) for 90 days. Significantly decreased magnetization transfer ratio (MTR) in the hippocampus of Al treated rats along with increased lipid and protein peroxidation. Ultrastructural steady also revealed that lipofuscin accumulation (a product of lipid peroxidation), demylination and disrupted nucleolar morphology in Al treated rats. B. monnieri significantly reversed Al induced morphological and biochemical changes. In conclusion, the study of the MTR profile, biochemical and ultrastructural study demonstrates in vivo the loss of neuronal lipid and proteins as evident by ultrastructural studies. This methodological approach can be applied to assessment of aluminum exposed patients to show neurodegeneration, should prove helpful to determine the degree of spontaneous and therapeutically induced regeneration and thus to validate therapeutic treatments for neuronal loss and repair.
Leptin concentrations are altered in favour of pro health after periodontal therapy. Leptin, a no... more Leptin concentrations are altered in favour of pro health after periodontal therapy. Leptin, a non-glycosylated peptide hormone, not only maintains fat stores, but is also an integral part of host defense repertoire. Leptin levels have been found to be altered in an array of inflammatory diseases including chronic periodontitis (CP), but the role of non-surgical periodontal therapy (NSPT) in altering the leptin concentrations in saliva and serum of CP patients is yet to be ascertained. The aim of the present study is to quantify leptin levels in CP patients having normal body mass index (BMI) pre-therapy as compared to periodontally healthy controls and to address whether successful NSPT alters leptin concentration in serum and saliva. Twenty-two saliva (modified draining method) and serum samples (by venipuncture) were collected from CP patients with normal BMI (n = 22), before and at 4 and 12 weeks after completion of NSPT, and periodontally healthy, age- and gender-matched controls (n = 22). Leptin levels were estimated using enzyme linked immunosorbent assay kits. At baseline, CP patients had significantly different periodontal clinical parameters and the leptin concentrations in saliva of CP patients were found to be significantly lower than periodontally healthy volunteers (4710.10 ± 1133.21 vs 8721.10 ± 1019.58 pg/ml) (p < 0.05), whereas in serum the leptin concentrations were significantly higher than healthy controls (10749 ± 2062.24 vs 8085.00 ± 2859.68 pg/ml). Significant improvement in periodontal parameters, serum and salivary leptin levels were observed in CP patients at 4 and 12 weeks post-therapy (p < 0.01). Altered concentrations of leptin in serum and saliva are observed in CP patients which can be restored in favor of health after periodontal therapy.
Background: The aim of this study is to investigate the impact of diabetes, a known risk factor f... more Background: The aim of this study is to investigate the impact of diabetes, a known risk factor for periodontitis, on activities of antioxidant enzymes superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) as well as levels of free radical damage marker malondialdehyde (MDA) in blood and saliva of individuals with chronic periodontitis (CP).Methods: Sixty patients with CP (30 patients with type 2 diabetes mellitus [DMCP] and 30 systemically healthy patients [CP]) and 60 periodontally healthy individuals (30 patients with type 2 diabetes mellitus and 30 systemically healthy patients [PH]) were included in this study. After clinical measurements, blood and saliva samples were collected. SOD, GR, and CAT activities in red blood cell lysate and saliva and MDA levels in plasma and saliva samples were spectrophotometrically assayed. An analysis of variance test followed by a post hoc test was used to compare the intragroup and intergroup variances among the study grou...
Induction of tumor necrosis factor-α (TNF-α) in response to lead (Pb) exposure has been implicate... more Induction of tumor necrosis factor-α (TNF-α) in response to lead (Pb) exposure has been implicated in its immunotoxicity. However, the molecular mechanism by which Pb upregulates the level of TNF-α is wagely known. An attempt was therefore made to elucidate the mechanistic aspect of TNF-α induction, mainly focusing transcriptional and post transcriptional regulation via mitogen activated protein kinases (MAPKs) activation. We observed that exposure of Pb to human monocytic THP-1 cells resulted in significant enhanced production of TNF-α m-RNA and protein secretion. Moreover, the stability of TNF-α m-RNA was also increased as indicated by its half life. Notably, activation of ERK 1/2, p38 and JNK in Pb exposed THP-1 was also evident. Specific inhibitor of ERK1/2, PD 98059 caused significant inhibition in production and stability of TNF-α m-RNA. However, SB 203580 partially inhibited production and stability of TNF-α m-RNA. Interestingly, a combined exposure of these two inhibitors completely blocked modulation of TNF-α m-RNA. Data tends to suggest that expression and stability of TNF-α induction due to Pb exposure is mainly regulated through ERK. Briefly, these observations are useful in understanding some mechanistic aspects of proinflammatory and immunotoxicity of Pb, a globally acknowledged key environmental contaminant.
American Journal of Neuroprotection and Neuroregeneration, 2013
ABSTRACT The aim of the present study was to time coarse assessment of aluminum chloride induced ... more ABSTRACT The aim of the present study was to time coarse assessment of aluminum chloride induced macromolecular changes by in vivo magnetization transfer brain imaging and therapeutic efficacies of Bacopa monnieri (BM) have been investigated. In the present study, 100 mg/kg of AlCl3 daily was administered orally to rats and co-administered with BM (40 mg/kg) for 90 days. Significantly decreased magnetization transfer ratio (MTR) in the hippocampus of Al treated rats along with increased lipid and protein peroxidation. Ultrastructural steady also revealed that lipofuscin accumulation (a product of lipid peroxidation), demylination and disrupted nucleolar morphology in Al treated rats. B. monnieri significantly reversed Al induced morphological and biochemical changes. In conclusion, the study of the MTR profile, biochemical and ultrastructural study demonstrates in vivo the loss of neuronal lipid and proteins as evident by ultrastructural studies. This methodological approach can be applied to assessment of aluminum exposed patients to show neurodegeneration, should prove helpful to determine the degree of spontaneous and therapeutically induced regeneration and thus to validate therapeutic treatments for neuronal loss and repair.
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Papers by Abbas Ali Mahdi