Non-steroidal anti-inflammatory drugs (NSAID) have long
been, and still, an essential group of drugs having anti-inflammatory,
antipyretic, and analgesic effects. The significant gastro-intestinal toxicity
associated with their use in treatment of
chronic arthritis remains of great
concern in clinical applications. The central pathogenic mechanism in
NSAID-induced gastro-duodenal toxicity lies in their ability to inhibit the
synthesis of prostaglandins by gastric mucosa through inhibition of cyclooxygenase
enzyme (Cox). There are two isoforms of Cox enzyme: Cox-1 and
Cox-2. The gastro-protective effects of prostaglandins are mediated by Cox-
1, while the inflammatory effects are mediated by Cox-2. NSAID lead to
inhibition of synthesis of prostaglandins, resulting in toxic effects on gastric
mucosa and beneficial anti-inflammatory effects.
This Study was designed to evaluate the effects of Aloe vacillans leaves juice
on carbon tetrachloride CCl4- induced hepatotoxicity in rats.
Hepatotoxicity was induced in rats by intraperitoneal (i.p) injection of CCl4 (1ml/kg) of body weight every
72h during ethanolic extract of Aloe vacillans
leaves were administrated at dose 250 mg/kg and 500 mg/kg of body weight
pass orally (p.o) daily for 14 days.
Twenty-four hours post-CCl4 treatment, blood samples were withdrawn
through retro orbital sinus.The hepatotoxicity and its prevention was assessed
by serum parameters like alanine aminotransferase (ALT), aspartate
aminotransferase (AST), total protein (T.P) and albumin (ALB).
دراسة تأثير الميتيل سلفونيل ميتان وخلاصة الشاي الأخضر في الوقاية من التهاب القولون التقرحي عند الجرذان
Many T2D use CAO as a laxative. We did not find sufficient research to explain CAO's potential effect on the levels of HbA1c in T2D patients. This study will study this effect. Rats (n=80) were divided into eight groups (n=10). Five groups (n=50) wer
e injected with streptozotocin intravenously to induce T2D. One group was given CAO with empagliflozin, and the second was assigned CAO only daily. The third was assigned CAO every two days, with empagliflozin, which was given daily. A fourth was assigned CAO alone daily. Also, the fifth was given empagliflozin alone. In the healthy groups, one group was given CAO, and the other was given empagliflozin. Also, the last healthy group was not assigned any drug. CAO's result on HbA1c in healthy rats was noted to decrease when delivered alone for eight weeks. HbA1c of the diabetic groups showed no significant difference (P-value<0.05) when comparing the rats given CAO with empagliflozin, and the rats were given CAO only. There was also no noticeable effect among the groups of rats given CAO daily and every two days. This study explains that CAO does not lead to a significant difference in HbA1c levels in diabetic rats, even it did for healthy rats, and if given alone, CAO could affect HbA1c levels if given over a long period. Also, CAO has a noticeable impact on experimental rats that co-administered Empagliflozin on HbA1c levels, and that Empagliflozin effect is not significantly affected if taken with CAO.
