بررسی ضایعات هیستوپاتولوژیک مغزی ناشی از توکسوپلاسما گوندی و شیزوفرنی القاء شده با کتامین در موش پس از درمان با سولفادیازین-تریمتوپریم

نوع مقاله : مقاله پژوهشی

نویسندگان

1 گروه انگل شناسی دامپزشکی، واحد کرج، دانشگاه آزاد اسلامی, کرج، ایران

2 عضو هیات علمی

چکیده

بیماری توکسوپلاسموزیس در انسان و حیوانات در اثر آلودگی با تک یاخته درون سلولی توکسوپلاسما گوندی ایجاد میشود که طی عفونت مزمن قادر بوده کیست های انگلی در بافت های مختلف علی الخصوص بافت مغز ایجاد کند. با توجه به اهمیت این بیماری که در واقع موجب تغییرات رفتاری هم سو با بیماری شیزوفرنی در انسان می شود، این مطالعه به بررسی و مقایسه این دو بیماری از لحاظ هیستوپاتولوژی پرداخته است. تعداد 60 موش نر BALB/c به طور تصادفی به 6 گروه ده تایی تقسیم شدند. گروه توکسوپلاسموز که با 103 تاکی زوآئیت از توکسوپلاسما گوندی آلوده شدند. گروه کتامین که با استفاده از کتامین با دوز 20 میلی­گرم بر کیلوگرم به مدت 14 روز القاء شیزوفرنی در آنها انجام گرفت. گروه توکسوپلاسموز و کتامین که بعد از هشت هفته از آلودگی موش­ها با توکسوپلاسما گوندی، القاء شیزوفرنی انجام شد. گروه توکسوپلاسموز و سولفادیازین و تری متوپریم که موش­ها هشت هفته پس از آلودگی با توکسوپلاسما گوندی، سولفادیازین و تری متوپریم را از طریق گاواژ خوراکی به ترتیب با دوزهای 100 و 2 میلی­گرم بر کیلوگرم به مدت 14 روز دریافت کردند. گروه توکسوپلاسموز، کتامین و سولفادیازین و تری متوپریم که موش­ها با توکسوپلاسما گوندی آلوده شدند و هشت هفته پس از عفونت، کتامین، سولفادیازین و تری متوپریم را به مدت  14 روز دریافت کردند. گروه کنترل که موش­ها نرمال سالین دریافت کردند. پس از یوتانایز موش­ها، مغز ها جداسازی شده و در فرمالین بافر 10 درصد نگهداری شد و به بخش پاتولوژی انتقال یافت و نمونه­های بافتی با ضخامت 5 میکرومتر زده شدند و با رنگ هماتوکسیلین و ائوزین رنگ آمیزی شدند. مشاهدات هیستوپاتولوژیک مربوط به مغز موش های گروه توکسوپلاسموز، حاکی از وجود کیست انگل، آپوپتوز نورون، گلیوز و نورون های ائوزینوفیلیک و التهاب اطراف عروقی و نکروز بافتی بوده است. در گروه شیزوفرن گلیوز و تغییرات نورودژنراتیو دیده شد. در گروه درمان شده کاهش کیست انگلی و سلول های التهابی نسبت به گروه آلوده دیده شد (P<0.05). تعداد کل سلول­ها اعم از نورون، آستروسیت و الیگودندروسیت در گروه کنترل با سایر گروه­ها دارای تفاوت معنادار (P<0.05) بوده است و این در حالیست که تعداد سلول­های میکروگلیا در بین گروه کنترل با گروه توکسوپلاسموز و توکسوپلاسموز-شیزوفرن معنادار بوده (P<0.05) و بین گروه­های کنترل و توکسوپلاسموز درمان شده و شیزوفرن معنادار نبوده است (P>0.05). تفاوت معناداری بین گروه های 2، 3، 4، 5 و 6 از جهت معناداری برای تعداد کل سلولهای شمارش شده، نورون و الیگودندروسیت وجود نداشته (P>0.05) و در مورد آستروسیت تفاوت معنادار تنها بین گروه های توکسوپلاسموز-شیزوفرن با گروه توکسوپلاسموز بوده است (P<0.05) و بین گروه های 2، 3، 5 و 6 تفاوت معنادار وجود نداشته و بین گروه های 2، 4، 5 و 6 نیز تفاوت معنادار وجود نداشته است (P>0.05). همچنین سایز نورون نیز در هیچکدام از گروه­ها معنادار نبوده است (P>0.05).
 

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

Histopathological investigating of brain lesions caused by Toxoplasma gondii and ketamine-induced schizophrenia in mice after treatment with sulfadiazine-trimethoprim

نویسندگان [English]

  • Seyedeh Mina i Masoum 1
  • Mohammadreza Youssefi 2
  • Seyed Shapoor Reza Shojaei 1
1 Department of Veterinary Parasitology, Karaj Branch, Islamic Azad University, Karaj, Iran
2 Department of Veterinary Parasitology, Babol Branch, Islamic Azad University, Babol, Iran
چکیده [English]

Toxoplasmosis is caused by the intracellular protozoan named, Toxoplasma gondii, in humans and animals. It is able to create parasitic cysts in various tissues during chronic infection, especially brain tissue. Considering the importance of this disease, which actually causes behavioral changes similar to schizophrenia in humans, this study is compared these two diseases based on histopathological analysis. 60 male BALB/c mice were randomly divided into 6 groups (10 mice in each group). Toxoplasmosis group is infected with 10³ tachyzoites of Toxoplasma gondii. The ketamine group is induced schizophrenia by ketamine at a dose of 20 mg/kg for 14 days. Toxoplasmosis and ketamine group is induced schizophrenia after eight weeks of infection with Toxoplasma gondii. Toxoplasmosis and sulfadiazine-trimethoprim group is received sulfadiazine and trimethoprim through oral gavage at doses of 100 and 2 mg/kg, respectively, for 14 days, eight weeks after infection with Toxoplasma gondii. Toxoplasmosis, ketamine, and sulfadiazine-trimethoprim group is infected with Toxoplasma gondii and received ketamine, sulfadiazine, and trimethoprim for 14 days after infection, eight weeks after infection with Toxoplasma gondii. The control group is received normal saline. After euthanizing, the brains were isolated and kept in 10% buffered formalin and transferred to the pathology department. Tissue samples were cut with a thickness of 5 micrometers and stained by hematoxylin and eosin. Histopathological observations of the toxoplasmosis group showed the presence of parasite cysts, neuron apoptosis, gliosis, eosinophilic neurons, perivascular cuffs, and tissue necrosis. Gliosis and neurodegenerative changes were seen in the schizophrenic group. In the treated group, there was a decrease in parasitic cysts and inflammatory cells compared to the infected group (P<0.05). The total number of cells including neurons, astrocytes and oligodendrocytes in the control group has a significant difference (P<0.05) with other groups, while the number of microglia cells between the control group and the toxoplasmosis and toxoplasmosis+ schizophrenia was significant (P<0.05) and between the control and toxoplasmosis treated groups, with schizophrenia was not significant (P>0.05). There was no significant difference between groups 2, 3, 4, 5 and 6 for the total number of counted cells, neurons and oligodendrocytes (P>0.05). According to astrocytes, there was a significant difference between the toxoplasmosis-schizophrenic groups and the toxoplasmosis group (P<0.05) and there was no significant difference between groups 2, 3, 5 and 6 and between groups 2, 4, 5 and 6. Also, the neuron size was not significant in any of the groups (P>0.05).
 

کلیدواژه‌ها [English]

  • Toxoplasma gondii
  • Schizophrenia
  • Mice
  • Histopathology
  • Sulfadiazine and Trimethoprim

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