Objective: Neuropathic pain (NP) is a chronic debilitating pain and is caused by disease or lesion of somatosensory system. NP respond worse to the pharmacological drugs leading to this pain still a big problem in medical treatment and furthermore make many patients seek alternative treatment. Wet cupping therapy (WCT) has been widely used to relief both of acute and chronic pain, but the mechanism for reducing pain has not yet been clear. Recent studies have shown that NP is associated with alteration of GLT-1/EAAT2, and WCT has beneficial role to reduce the pain in various pain models. This is the pilot study, no other study has applied WCT in chronic constriction injury (CCI) models, the most commonly employed animal model of NP. Therefore, we investigate the association between WCT and the reducing pain by looking at the increase of GLT-1 and time withdrawal latency (TWL) in rats with CCI. Methodology: The study design was randomized, post-test only, controlled trial with a total of 21 male rats (Rattus Norvegicus) with CCI, aged 4 months, weighing 220 to 250 g, randomly divided into three groups, P1 (sham CCI group), P2 (CCI group), and P3 (CCI group plus WCT). WCT had been applied 2 times/week for 3 weeks to all of the groups in paralumbar region, both left and right side. TWL was recorded to assess pain threshold of the rats by hot plate and the expression of GLT-1 on glial cells in spinal cord were counted. Results: This study revealed that mean ± SD values for P1, P2, and P3 were 7.20 ± 1.30, 2.57 ± 1.27, and 18.20 ± 3.50 respectively. There were significant differences in the TWL between groups P1-P2, P1-P3, and P2-P3 (p = 0.003, p = 0.0001, and p = 0.0001 respectively) and GLT-1 increase was significant between groups P2-P3 (p =  0.009). Conclusion: It can be concluded that wet cupping therapy decreases the pain by increasing the time withdrawal latency and GLT-1 in chronic constriction injury models. We suggest that wet cupping therapy as a promising method to reduce pain in peripheral neuropathic pain models. However, further investigation is still needed to confirm its mechanism of action. Key words: GLT-1/EAAT2; Neuropathic pain; Wet cupping therapy; Chronic constriction injury; CCI, TWL Citation: Hidayati HB, Machfoed MH, Kuntoro, Subadi I, Khaerunnisa S, Widjiati. Increase in the glutamate transporter 1 and time withdrawal latency following wet cupping therapy in chronic constriction injury in rats. Anaesth. pain & intensive care 2021;25(1):48-54. DOI: 10.35975/apic.v25i1.1441 Received: 24 January 2019, Reviewed: 4 January 2019, 14 January 2019, Revised: 24 January 2019, Accepted: 20 May 2019

Introduction The aim of the study was to describe the process of neuron death in the cerebral cortex caused by embryonic carbofuran exposure. Material and Methods 81 mouse foetuses from 27 breeding mice were used in the study. Carbofuran was administered by gavage from the 6th to the 15th day of gestation to two groups: one at 0.0208 and the other at 0.0417 mg/kg b.w. On the 17th day, the mice were sacrificed and the foetuses were taken to measure the ROS (malondialdehyde/MDA and superoxide dismutase/SOD) activity in brain tissue, the number of apoptotic embryonic cerebral cortex neurons using a TUNEL assay, and necrotic cells using HE staining. Examination of p53 and caspase 3 expression was done by immunohistochemistry. Data were analysed using analysis of variance (ANOVA) and Duncan’s test. Results Increased activity of cerebral ROS characterised by significant elevation of the MDA level (P < 0.05), decreased SOD (P < 0.01), increased p53 and caspase 3 expression, and cerebral cortical neuron death either by necrosis or apoptosis (P < 0.05) were found. At the low dose carbofuran increased expression of p53, caspase 3, and apoptosis. At the high dose it increased levels of MDA and necrosis. Conclusion Increased expression of p53 and caspase 3 and apoptosis indicated that carbofuran may cause apoptosis through the intrinsic pathway. The increased apoptosis grants an opportunity to prevent and treat the effect of ROS due to gestational carbofuran exposure.

Background Polycystic ovary syndrome (PCOS) is a syndrome characterized by ovulation disorders accompanied by hyperandrogens. Women with PCOS are prone to develop insulin resistance which has metabolic characteristics similar to type 2 diabetes and leads to disturbance of follicular formation. PCOS is also known to increase the concentration of proinflammatory cytokines, namely TNF-α. Moringa oleifera leaves have been shown to have compounds that can reduce insulin levels and glucose levels in diabetes mellitus and should be able to reduce TNF-α and follicle count. Purpose This study aims to prove the effectiveness of Moringa oleifera leaf in reducing insulin, glucose levels, TNF-α and follicle count in PCOS. Methods The three-month-old white rats Wistar ( Rattus norvegicus ) 150–170 grams were divided into four groups (n = 10), namely normal rats, PCOS model rats, PCOS model rats given metformin, and PCOS rats given 500mg of Moringa oleifera . The method of this study is taking PCOS model rats by injecting the 100mg/kg BW hormone testosterone propionate for 21 days. After 21 days of therapy, we analyzed insulin, glucose levels, TNF-α and follicle count. Results The PCOS control group showed an increase in insulin level, glucose levels, TNF-α expression, and a decrease in the follicle count compared to the normal control group. The insulin level, glucose level, TNF-α and follicle count in the Moringa oleifera 500 mg/kg BW treatment group were significantly lower than in the PCOS control group. Conclusion Moringa oleifera leaves have the potential in reducing insulin levels, blood glucose levels, TNF-α and follicle count in PCOS patients.

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Background and Aim: Endometriosis affects the ovaries and causes a decrease in the oocyte quality during endometrial receptivity. During the development of ovarian follicles, paracrine communication occurs between granulosa cells and oocytes. This study was conducted to determine the effects of bone marrow mesenchymal stem cell transplantation on tumor necrosis factor-alpha (TNF-α) receptor 1 (TNFR1) expression, granulosa cell apoptosis, and folliculogenesis in endometriosis mouse models. Materials and Methods: This study involved 42 female mice, which were divided into three groups: Healthy mice (T0), endometriosis mice without transplantation (T1), and endometriosis mice with bone marrow mesenchymal stem cell transplantation (T2). The mice were injected intraperitoneally with endometrial fragments (200 μL) to become endometriosis models. On day 15, the endometriosis models received mesenchymal stem cells. Sample collection was performed on day 29. Granulosa cell apoptosis and TNFR1 expression were examined using immunohistochemical staining, and folliculogenesis was assessed using hematoxylin and eosin staining of ovary samples. The data obtained from both examinations were statistically analyzed using Statistical Package for the Social Sciences. Results: The results showed that TNFR1 expression is significantly decreased in T2 (p<0.004). The apoptosis of granulosa cells was lower in T2 (p<0.000). The primary, secondary, and graafian follicle counts in T2 were significantly increased. Conclusion: Bone marrow mesenchymal stem cell transplantation in endometriosis mouse models can reduce TNFR1 expression and granulosa cell apoptosis and improve folliculogenesis.