Journal of

Introduction: Various lesions trigger an inflammatory response in the host body. These injuries include surgical stress Surgery exerts stress on the body. Systemic inflammatory syndrome is a reflection of the degree of surgical stress and as a system of assessing the severity of postoperative stress. Regular complexes of inflammatory polypeptide molecules contribute to the development of this inflammatory response known as cytokines. Lack of local control over the release of these cytokines can cause systemic inflammation, and potentially devastating complications.
In writing this review articles, articles indexed in the following databases were used: Science Direct, Scopus, Springer Science, PubMed and Google Scholar Ninety two related research papers, including quantitative and qualitative researches in English, related to the last 40 years (1979- 2019) were included in this study. The current review article has been written based on 92 articles and the keywords of “Surgical Stress, Systemic Inflammatory Response Syndrome, Pro-Inflammatory Cytokines, and Anti-Inflammatory Cytokines”.
Studies in humans and animal models suggest that both types of pro-inflammatory and anti-inflammatory cytokines following diverse primary stimuli, including endotoxin release, complement system activation, ischemia-perfusion injury, and other ways.
Conclusion: Inflammatory and anti-inflammatory cytokines are the result of a complex unpredictable interaction of immune system effects on the body and even multiple effects on body organs. New therapeutic strategies for the absorption of cytokines are a powerful way to enhance and improve proper output, following systemic inflammatory response syndrome.

Introduction: Spinal cord injury (SCI) causes devastating injuries in patients. The main mechanisms of the pathogenesis of secondary injury include nerve degeneration, gliosis, and inflammation. Spinal cord injury induces a disorder or failure in several organs due to the vital role of the spinal cord in regulating bodily functions. Osteoporosis is a consequence of spinal cord injury that occurs in the vast majority of patients with spinal cord injury.
Articles on the related topic were searched in the following databases: Science Direct, Scopus, Springer Science, PubMed and Google scholar to have been used in writing from this review article. A total of 120 related research papers, including quantitatve and qualitative researches in English, from the last 57 years papers (1962- 2019) were included in this study. The review article is written according to 120 articles and the keywords “Spinal cord injury, Osteoporosis, Inflammation, Osteoblast and Osteoclast”.
Conclusion: Although weight loss is an important factor in the development of osteoporosis following SCI, inflammation, nerve damage, and hormonal changes also contribute to this process. Hormonal changes mediated by SCI may contribute to postoperative osteoporosis with several mechanisms. These mechanisms included: increased renal excretion and decreased intestinal absorption of calcium, consequently, a negative balance of calcium ions; Vitamin D deficiency; impair the function of the gonads and inhibits the osteoanabolic (ossification) activity of sex steroids; elevated blood leptin; Pituitary suppression of parathyroid hormone, and bone loss following SCI may (at least in part) be caused directly by insulin resistance and insulin-like growth factor.

Introduction: Endometriosis is one of the main causes of pelvic pain and subfertility, which is characterized by endometrial-like tissues outside the uterus and primarily is created in the pelvic peritoneum, ovaries, walls between the rectum and vagina and in rare cases in the diaphragm, pleura and pericardium. Some risk factors for endometriosis are obstruction in menstrual hemorrhage, an increase in the duration of endogenous estrogen, short menstrual cycles and childbirth at an early age. On the other hand, osteoporosis is a metabolic disease that is determined by bone mineral density and the destruction of the bone microstructure that increases the risk of bone fracture. About 200 million people worldwide are suffering from osteoporosis, that 34% of them are women over 50 years old. The first and most commonly used model for the induction of this disease is the ovariectomy model in rats, which gives a model of the relationship between osteoporosis and menopause.
Conclusion: Endometriosis animal models are highly contributing to the development of new non-invasive diagnostic tools and improve therapeutic methods for treatment of endometriosis in women. Although no animal models are absolutely ideal and excellent, but the presence of many similarities in the response of the human skeletal system and rats to reduce estrogen levels and therapeutic compounds caused by the ovariectomy model of the rat, a suitable model for osteoporosis research. The response of rat bones to ovariectomy depends on the type of bone (trabecular against cortical), bone sites (femur, proximal Tibia, and lumbar vertebrae) and it depends on the time elapsed after ovariectomy (the time required to reduce the amount of estrogen levels).

Introduction: Endometritis is a female reproductive disease characterized by the inflammation of the endometrial glandular and stromal tissues. It is usually occurred due to uterine contamination with infectious causes. Animal models of clinical endometritis are very important to prevent the incidence and treatment of endometritis. Vaginal cytology method is considered as a golden standard for determining the estrous cycle stage in female rats. The aim of this study was to induce endometritis in a rat model and determine the stages of the estrous cycle of this animal using vaginal cytology method in order to successfully induce this condition in this animal model.
Conclusion: Inflammation changes the production of endometrial cytokines, which may result in menstrual disorders and decreased endometrial reception by impaired endometrial tissue dysfunction. Increased expression of specific cytokines genes such as IL-6, IL-8 and TNF-α can be used to detect the severity and degree of endometritis. Uterine infections are known as a result of damage to the defense mechanisms of the uterine tissue, which are caused by physiological changes in the postpartum period. Another change that occurs in the postpartum period is the increase in the production of reactive oxygen species. The imbalance between the production of reactive oxygen species and its clearance leads to the creation of oxidative stress conditions. On the other hand, there is a significant relationship between inflammatory diseases such as endometritis and oxidative stress. On other hand, by accurately determining the estrous cycle of rats by using vaginal cytology, endometritis can be well induced in this species.