المؤلفون: Perveen, Hasina, Chattopadhyay, Sandip, Maity, Moulima, Dash, Moumita, Islam, Syed Sirajul

المصدر: Journal of Basic & Clinical Physiology & Pharmacology; Jul2019, Vol. 30 Issue 4, pN.PAG-N.PAG, 14p

مصطلحات موضوعية: ADENOSYLMETHIONINE, ANIMAL experimentation, ARSENIC compounds, BIOMARKERS, CATALASE, CYTOKINES, FOLIC acid, FREE radicals, GENE expression, OVARIAN follicle, INTERLEUKINS, LACTATE dehydrogenase, LIVER, METALLOPROTEINS, NECROSIS, ORAL drug administration, PEROXIDASE, RATS, SODIUM compounds, SUPEROXIDE dismutase, TUMOR necrosis factors, UTERUS, UTERINE diseases, VITAMIN B12, HOMOCYSTEINE, DNA-binding proteins, ANDROSTENEDIONE, OXIDATIVE stress, CURCUMIN

مستخلص: Background: Curcumin is extensively used as a therapeutic intervention for treating several ailments. The antioxidant curcumin has an anti-inflammatory and chelating property with arsenic to exhibit a strong therapeutic effect on reproductive organs. This study was undertaken to describe the protective effect of noninvasive administration of curcumin against sodium-arsenite-mediated uterine hazards in female Wistar rats. Methods: Twenty-four female Wistar rats were randomly divided into four groups. The treatment was continued for 8 days and given orally sodium arsenite (10 mg/kg body weight) in combination with curcumin (20 mg/kg body weight). Results: Our evaluation revealed that 8 days of sodium arsenite (10 mg/kg body weight) treatment reduced the activities of the uterine enzymatic antioxidants superoxide dismutase, catalase, and peroxidase. Blood levels of vitamin B12 and folic acid decreased followed by an increased serum lactate dehydrogenase, homocysteine level, and hepatic metallothionein-1 in arsenic-treated rats. Necrosis of uterine tissue along with the disruption of ovarian steroidogenesis was marked in arsenic-treated rats with an upregulation of uterine NF-κB and IL-6 along with a raised level of serum TNF-α. Oral administration of curcumin (20 mg/kg body weight/day) in arsenic-treated rats significantly reinstated these alterations of the antioxidant system followed by an improvement of ovarian steroidogenesis and the circulating level of B12 and folate along with the downregulation of serum homocysteine, metallothionein-1, and cytokines. Conclusions: The findings of this study clearly and strongly elucidated that arsenic-induced oxidative stress in uterus is linked to an alteration of inflammation-signaling biomarkers and these have been protected through the co-administration of curcumin due to its anti-inflammatory, free radical scavenging, and antioxidant activity by the possible regulation of an S-adenosine methionine pool. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Basic & Clinical Physiology & Pharmacology is the property of De Gruyter and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Meena, Shaikh Zohra, Rahman, Md. Azizur, Bagga, Paramdeep, Mujahid, Md.

المصدر: Journal of Basic & Clinical Physiology & Pharmacology; Jan2019, Vol. 30 Issue 1, p131-137, 7p

مصطلحات موضوعية: ALKALINE phosphatase, ANIMAL experimentation, ASPARTATE aminotransferase, BARK, BILIRUBIN, BIOMARKERS, BODY weight, CELLULOSE, COMBINATION drug therapy, CHOLESTEROL, ETHANOL, FLAVONOIDS, HISTOLOGICAL techniques, ISONIAZID, LACTATE dehydrogenase, LIVER, LIVER diseases, ORAL drug administration, PEPTIDES, RATS, RIFAMPIN, PLANT stems, PLANT extracts, ALBUMINS, ALANINE aminotransferase

مستخلص: Background: Development of drug-induced hepatic damage (DIHD) during chemotherapy is the most common reason for interruption in chemotherapy. This study evaluated the hepatoprotective activity of the ethanolic extract of Tamarindus indica stem bark (EETI) against the induced DIHD in Sprague Dawley rats. Methods: The rats were divided into five groups (n=5). Group I, group III, group IV, and group V rats received 1 mL 1% carboxymethyl cellulose, EETI 100 mg/kg body weight (b.wt), EETI 200 mg/kg b.wt, and silymarin 100 mg/kg b.wt, respectively, orally once every day for 28 days. After 1 h–group II, group III, group IV, and group V rats were administered with isoniazid (INH) and rifampicin (RIF) 50 mg/kg b.wt each orally once every day for 28 days. Then, 24 h after the last dosing, blood was withdrawn from the rats and analyzed for liver specific enzymes and biochemical markers. They were examined for histopathology. Results: Co-administration of INH and RIF in group II significantly increased alanine transaminase, aspartate transaminase, alkaline phosphatase, lactate dehydrogenase, serum bilirubin, and cholesterol levels while reduced the total protein and albumin levels compared to that of group I. EETI in group III and group IV rats significantly restored the liver specific enzymes and biochemical markers altered due to co-administration of INH and RIF to normal in a dose-dependent manner. EETI 200 mg/kg b.wt showed better protection to liver than EETI 100 mg/kg b.wt and was comparable to silymarin 100 mg/kg b.wt. It was well supported with histopathology of liver tissues. Conclusions: EETI possesses hepatoprotective activity against DIHD in rats. It may have a substantial impact on developing clinical strategies to treat patients with hepatic damage. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Basic & Clinical Physiology & Pharmacology is the property of De Gruyter and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)