Parkinson's disease (PD) is characterized by the ... more Parkinson's disease (PD) is characterized by the progressive degeneration via apoptosis of nigrostriatal dopaminergic neurons associated with inflammation, resulting in behavioral anomalies. Therefore, an anti-apoptotic and anti-inflammatory regimen may be useful in treatment of PD. CNB-001, a novel pyrazole derivative of curcumin and cyclohexyl bisphenol A has superior biological properties than its parental compounds. The present study utilizes a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate anti-inflammatory and anti-apoptotic mediated neuroprotection of CNB-001. The administration of MPTP (30 mg/kg for four successive days) significantly induced motor impairments as determined by behavioral studies (narrow beam test, catalepsy and akinesia), lowered dopamine levels and up-regulated the expressions of the inflammatory and apoptotic markers (tumor necrosis factor-alpha, interleukin-1β, interleukin-6, inducible nitric oxide synthase, glial fibrillary acidic protein, cyclooxygenase-2 and Bax). Moreover, MPTP treatment attenuated Bcl-2 and nigrostriatal dopamine transporter expression and also increased total nitrite and citrulline levels in comparison to the control group. However, co-treatment with CNB-001 significantly attenuated motor impairments and pathological changes caused by MPTP administration. Collectively, our results demonstrate that CNB-001 is neuroprotective through its anti-inflammatory and anti-apoptotic properties. Thus, CNB-001 has potential to be further developed as a therapeutic candidate for treatment of PD.
ABSTRACT Purpose Ulcerative colitis (UC) is associated with tainted neutrophil infiltration, dere... more ABSTRACT Purpose Ulcerative colitis (UC) is associated with tainted neutrophil infiltration, deregulated pro-inflammatory mediators, characterized by severe oxidative stress of the intestine. In the present study, an effort was made to evaluate the effect of methanolic fractions of Eupatorium triplinerve (E. triplinerve) (ET) on acetic acid induced ulcerative colitis in male adult mice. Methods Colitis in mice was induced with 3.0% acetic acid (v/v) in saline via rectal route. Pre-intervention with E. triplinerve extract (100 mg and 200 mg kg−1 body weight, oral) and reference drug ranitidine (50 mg kg−1 body weight used as reference, oral) 4 days before induction of colitis and was extended up to 8 days. Results The phase of inflammation before E. triplinerve extract pre-treatment significantly showed attenuated macroscopic damage, argyrophilic nuclear organization regions (AgNORs) count and histological changes. Similarly, extract also effectively detracts the activity of both Myeloperoxidase (MPO) and Malondialdehyde (MDA) levels by enhancing the cellular antioxidant enzyme levels (Glutathione-s-transferase [GST], Glutathione peroxidise [GPx] and Catalase [CAT]) at the site of ulceration. Conclusions The E. triplinerve based therapy resolved that some constituents in extract have an antiulcer effect against UC at colon specific area through its inviolable radical scavenging activity.
New strategies for the prevention of colon cancer persists a crucial need. However, resistance to... more New strategies for the prevention of colon cancer persists a crucial need. However, resistance to current chemopreventive drugs is relatively prevalent in colon carcinogenesis. For this intent, a chemopreventive study was acquitted to elucidate the probable effect of taxifolin (TAX) against 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis in mice and to evaluate its efficacy with 5-fluorouracil (5-FU) drug control. Swiss Albino mice were intended for colon carcinogenesis received subcutaneous injections of DMH (20 mg/kg bw., sc) once a week for 15 weeks and were treated with TAX (4 g/kg bw, op) and 5-FU drug control (10 mg/kg bw., op) for the entire study period. Our results unveil that mice administered with TAX significantly modulates DMH induced histological alterations (ACF, AgNORs, and mucin depletion). Moreover, TAX treatment also inhibits DMH mediated oxidative damage by diminishing tissue lipid peroxidation (MDA, MPO and CD) accompanied by enhanced activities of enhanced activities of free radical metabolizing enzymes (SOD, CAT, GPx, GR, GSH, vitamin A, C and E). Apoptotic and proliferating cell nuclear antigen (PCNA) findings also revealed that treatment with TAX substantially regulates cell proliferation through the increased extent of DNA fragmentation. The incidence of colon cancer in TAX treated mice was significantly reduced when compared to that of 5-FU control. Our findings concluded that taxifolin act as an effective chemopreventive agent against colon carcinogenesis by its virtue of antioxidant mediated apoptosis and anti-proliferative activities.
Parkinson's disease (PD) is characterized by the ... more Parkinson's disease (PD) is characterized by the progressive degeneration via apoptosis of nigrostriatal dopaminergic neurons associated with inflammation, resulting in behavioral anomalies. Therefore, an anti-apoptotic and anti-inflammatory regimen may be useful in treatment of PD. CNB-001, a novel pyrazole derivative of curcumin and cyclohexyl bisphenol A has superior biological properties than its parental compounds. The present study utilizes a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD to investigate anti-inflammatory and anti-apoptotic mediated neuroprotection of CNB-001. The administration of MPTP (30 mg/kg for four successive days) significantly induced motor impairments as determined by behavioral studies (narrow beam test, catalepsy and akinesia), lowered dopamine levels and up-regulated the expressions of the inflammatory and apoptotic markers (tumor necrosis factor-alpha, interleukin-1β, interleukin-6, inducible nitric oxide synthase, glial fibrillary acidic protein, cyclooxygenase-2 and Bax). Moreover, MPTP treatment attenuated Bcl-2 and nigrostriatal dopamine transporter expression and also increased total nitrite and citrulline levels in comparison to the control group. However, co-treatment with CNB-001 significantly attenuated motor impairments and pathological changes caused by MPTP administration. Collectively, our results demonstrate that CNB-001 is neuroprotective through its anti-inflammatory and anti-apoptotic properties. Thus, CNB-001 has potential to be further developed as a therapeutic candidate for treatment of PD.
ABSTRACT Purpose Ulcerative colitis (UC) is associated with tainted neutrophil infiltration, dere... more ABSTRACT Purpose Ulcerative colitis (UC) is associated with tainted neutrophil infiltration, deregulated pro-inflammatory mediators, characterized by severe oxidative stress of the intestine. In the present study, an effort was made to evaluate the effect of methanolic fractions of Eupatorium triplinerve (E. triplinerve) (ET) on acetic acid induced ulcerative colitis in male adult mice. Methods Colitis in mice was induced with 3.0% acetic acid (v/v) in saline via rectal route. Pre-intervention with E. triplinerve extract (100 mg and 200 mg kg−1 body weight, oral) and reference drug ranitidine (50 mg kg−1 body weight used as reference, oral) 4 days before induction of colitis and was extended up to 8 days. Results The phase of inflammation before E. triplinerve extract pre-treatment significantly showed attenuated macroscopic damage, argyrophilic nuclear organization regions (AgNORs) count and histological changes. Similarly, extract also effectively detracts the activity of both Myeloperoxidase (MPO) and Malondialdehyde (MDA) levels by enhancing the cellular antioxidant enzyme levels (Glutathione-s-transferase [GST], Glutathione peroxidise [GPx] and Catalase [CAT]) at the site of ulceration. Conclusions The E. triplinerve based therapy resolved that some constituents in extract have an antiulcer effect against UC at colon specific area through its inviolable radical scavenging activity.
New strategies for the prevention of colon cancer persists a crucial need. However, resistance to... more New strategies for the prevention of colon cancer persists a crucial need. However, resistance to current chemopreventive drugs is relatively prevalent in colon carcinogenesis. For this intent, a chemopreventive study was acquitted to elucidate the probable effect of taxifolin (TAX) against 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis in mice and to evaluate its efficacy with 5-fluorouracil (5-FU) drug control. Swiss Albino mice were intended for colon carcinogenesis received subcutaneous injections of DMH (20 mg/kg bw., sc) once a week for 15 weeks and were treated with TAX (4 g/kg bw, op) and 5-FU drug control (10 mg/kg bw., op) for the entire study period. Our results unveil that mice administered with TAX significantly modulates DMH induced histological alterations (ACF, AgNORs, and mucin depletion). Moreover, TAX treatment also inhibits DMH mediated oxidative damage by diminishing tissue lipid peroxidation (MDA, MPO and CD) accompanied by enhanced activities of enhanced activities of free radical metabolizing enzymes (SOD, CAT, GPx, GR, GSH, vitamin A, C and E). Apoptotic and proliferating cell nuclear antigen (PCNA) findings also revealed that treatment with TAX substantially regulates cell proliferation through the increased extent of DNA fragmentation. The incidence of colon cancer in TAX treated mice was significantly reduced when compared to that of 5-FU control. Our findings concluded that taxifolin act as an effective chemopreventive agent against colon carcinogenesis by its virtue of antioxidant mediated apoptosis and anti-proliferative activities.
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chemopreventive drugs is relatively prevalent in colon carcinogenesis. For this intent, a chemopreventive
study was acquitted to elucidate the probable effect of taxifolin (TAX) against 1,2-dimethylhydrazine
(DMH) induced colon carcinogenesis in mice and to evaluate its efficacy with 5-fluorouracil (5-FU) drug
control. Swiss Albino mice were intended for colon carcinogenesis received subcutaneous injections of
DMH (20 mg/kg bw., sc) once a week for 15 weeks and were treated with TAX (4 g/kg bw, op) and 5-FU
drug control (10 mg/kg bw., op) for the entire study period. Our results unveil that mice administered with
TAX significantly modulates DMH induced histological alterations (ACF, AgNORs, and mucin depletion).
Moreover, TAX treatment also inhibits DMH mediated oxidative damage by diminishing tissue lipid
peroxidation (MDA, MPO and CD) accompanied by enhanced activities of enhanced activities of free
radical metabolizing enzymes (SOD, CAT, GPx, GR, GSH, vitamin A, C and E). Apoptotic and proliferating
cell nuclear antigen (PCNA) findings also revealed that treatment with TAX substantially regulates cell
proliferation through the increased extent of DNA fragmentation. The incidence of colon cancer in TAX
treated mice was significantly reduced when compared to that of 5-FU control. Our findings concluded
that taxifolin act as an effective chemopreventive agent against colon carcinogenesis by its virtue of
antioxidant mediated apoptosis and anti-proliferative activities.
chemopreventive drugs is relatively prevalent in colon carcinogenesis. For this intent, a chemopreventive
study was acquitted to elucidate the probable effect of taxifolin (TAX) against 1,2-dimethylhydrazine
(DMH) induced colon carcinogenesis in mice and to evaluate its efficacy with 5-fluorouracil (5-FU) drug
control. Swiss Albino mice were intended for colon carcinogenesis received subcutaneous injections of
DMH (20 mg/kg bw., sc) once a week for 15 weeks and were treated with TAX (4 g/kg bw, op) and 5-FU
drug control (10 mg/kg bw., op) for the entire study period. Our results unveil that mice administered with
TAX significantly modulates DMH induced histological alterations (ACF, AgNORs, and mucin depletion).
Moreover, TAX treatment also inhibits DMH mediated oxidative damage by diminishing tissue lipid
peroxidation (MDA, MPO and CD) accompanied by enhanced activities of enhanced activities of free
radical metabolizing enzymes (SOD, CAT, GPx, GR, GSH, vitamin A, C and E). Apoptotic and proliferating
cell nuclear antigen (PCNA) findings also revealed that treatment with TAX substantially regulates cell
proliferation through the increased extent of DNA fragmentation. The incidence of colon cancer in TAX
treated mice was significantly reduced when compared to that of 5-FU control. Our findings concluded
that taxifolin act as an effective chemopreventive agent against colon carcinogenesis by its virtue of
antioxidant mediated apoptosis and anti-proliferative activities.