Zingiber officinale alters 3,4-methylenedioxymeth amphetamine-induced neurotoxicity in rat brain

The spice Zingiber officinale or ginger possesses antioxidant activity and neuroprotective effects. The effects of this traditional herbal medicine on 3,4-methylenedioxymethamphetamine [MDMA] induced neurotoxicity have not yet been studied. The present study considers the effects of Zingiber officinale on MDMA-induced spatial memory impairment and apoptosis in the hippocampus of male rats. In this experimental study, 21 adult male Sprague Dawley rats [200-250 g] were classified into three groups [control, MDMA, and MDMA plus ginger]. The groups were intraperitoneally administered 10 mg/kg MDMA, 10 mg/kg MDMA plus 100 mg/kg ginger extract, or 1 cc/kg normal saline as the control solution for one week [n=7 per group]. Learning memory was assessed by Morris water maze [MWM] after the last administration. Finally, the brains were removed to study the cell number in the cornu ammonis [CA1] hippocampus by light microscope, Bcl-2 by immunoblotting, and Bax expression by reverse transcription polymerase chain reaction [RT-PCR]. Data was analyzed using SPSS 16 software and a one-way ANOVA test. Escape latency and traveled distances decreased significantly in the MDMA plus ginger group relative to the MDMA group [p<0.001]. Cell number increased in the MDMA plus ginger group in comparison to the MDMA group. Down-regulation of Bcl-2 and up-regulation of Bax were observed in the MDMA plus ginger group in comparison to the MDMA group [p<0.05]. Our findings suggest that ginger consumption may lead to an improvement of MDMA-induced neurotoxicity

role of the A2A receptor in cell apoptosis caused by MDMA

Ecstasy, also known as 3, 4-methylenedioxymethamphetamine [MDMA], is a psychoactive recreational hallucinogenic substance and a major worldwide recreational drug. There are neurotoxic effects observed in laboratory animals and humans following MDMA use. MDMA causes apoptosis in neurons of the central nervous system [CNS]. Withdrawal signs are attenuated by treatment with the adenosine receptor [A2A receptor]. This study reports the effects of glutamyl cysteine synthetase [GCS], as an A2A receptor agonist, and succinylcholine [SCH], as an A2A receptor antagonist, on Sprague Dawley rats, both in the presence and absence of MDMA. In this experimental study, we used seven groups of Sprague Dawley rats [200-250 g each]. Each group was treated with daily intraperitoneal [IP] injections for a period of one week, as follows: i. MDMA [10 mg/kg]; ii. GCS [0.3 mg/kg]; iii. SCH [0.3 mg/kg]; iv. GCS + SCH [0.3 mg/kg each]; v. MDMA [10 mg/kg] + GCS [0.3 mg/kg]; vi. MDMA [10 mg/kg] + SCH [0.3 mg/kg]; and vi. normal saline [1 cc/kg] as the sham group. Bax [apoptotic protein] and Bcl-2 [anti-apoptotic protein] expressions were evaluated by striatum using RT-PCR and Western blot analysis. There was a significant increase in Bax protein expression in the MDMA+SCH group and a significant decrease in Bcl-2 protein expression in the MDMA+SCH group [p<0.05]. A2A receptors have a role in the apoptotic effects of MDMA via the Bax and Bcl-2 pathways. An agonist of this receptor [GCS] decreases the cytotoxcity of MDMA, while the antagonist of this receptor [SCH] increases its cytotoxcity

Induction of endometriosis by implantation of endometrial fragments in female rats

Endometriosis is defined as the growth of endometrial tissues in ectopic places outside the uterus. This disease has an important effect on the health and fertility of affected women. It's etiology is not clearly known. For better understanding the pathophysiology of this disease, many researchers study on several aspects of the disease on animals. In this experimental study endometriosis was induced in female rats surgically and then its side effects were investigated with special focus on adhesion formation that is a major problem in women with this disease. In Protestrous phase, female rats were randomly divided into two groups. In both groups, under intra peritoneal anesthesia, laparotomy was done and left horn and associated fat were removed. In experimented group [A], the removed endometrium was cut to six square pieces [2mm each] and they were sutured to the peritoneum, near ovaries and subcutaneous. In sham group [B], the same procedure was done for the fat tissues around the removed horn and the pieces were sutured to the same places. After 8 weeks, in Protestrous phase, clinical adhesion and size of implants were evaluated. The total mean size of implants was calculated in each group, and this was significantly larger in experimented group [25.4 mm versus 2 mm p=0.000]. The mean diameter of implants that calculated for each site of implantation in experimented group were significantly larger in left peritoneum [p=0.002], followed by right [p=0.000] and left [p=0.000] ovaries. The endometrial tissues grew in 100% of implants in subcutaneous area. Clinical adhesions [Score. 2] were detected in 7 out of 10 in experimented group and in 2 out 10 in control group. The number of Esterous cycle were similar in both groups. Our study showed that after inducing endometriosis by surgical approach, only endometrial implants grew as a cystic structures and this is a unique aspect of endometrial cells. Our results showed that endometriosis had a direct effect on adhesion formation, not surgery alone and induction of this disease didn't have any adverse effect on ovarian function in female rats