2488 Indian Journal of Forensic Medicine & Toxicology, April-June 2021, Vol. 15, No. 2 Green Tea Suppresses Serum TNF-α and TGF-β1 Levels In Mice Model of Systemic Lupus Erythematosus Herin Mawarti 1,5 , Jusak Nugraha 2 , Djoko Agus Purwanto 3 , Joewono Soeroso 4 1 Doctoral Student. Doctoral Program of Medical Science, Faculty of Medicine, Airlangga University, Indonesia, 2 Professsor, Department of Clinical Patology, Faculty of Medicine, Airlangga University, Indonesia, 3 Professsor, Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Airlangga University, Indonesia, 4 Professsor, Department of Internal Medicine, Faculty of Medicine, Airlangga University, Indonesia, 5 Assistant Professor, Department of Nursing Science, Faculty of Health Sciences, University of Pesantren Tinggi Darul Ulum, Jombang, Indonesia Abstract Objective: This study aims to investigate the effects of green tea administration on TNF-a, Hsp70, and TGF-b1 levels in the systemic lupus erythematosus (SLE). Material and methods: A total of 32 mice will be divided into four groups (each 8 mice), namely the control group, the SLE group, the SLE group who were given green tea extract at a dose of 500 mg/kg body weight, and the SLE group who were given green tea extract at a dose of 1000 mg/kg body weight. Analysis of TNF-a, Hsp70, and TGF-b1 levels was carried out using the enzyme-linked immunosorbent assay technique. Results: TNF-a and TGF-b1 levels were signifcantly increased in the SLE group compared to the control group (p < 0.05). This increase can be signifcantly reduced through the provision of green tea, even reaching levels comparable to the control group (p > 0.05). Conclusions: It was concluded that green tea containing EGCG can suppress TNF-a and TGF-b1 in the SLE model. Thus, green tea can be an alternative in immunology modulation in SLE. Keywords: green tea; SLE; infammation; EGCG; stress protein Introduction Systemic lupus erythematosus (SLE) is complex autoimmune and infammatory disease marked by the presence of autoantibodies against nuclear and cytoplasmic antigens [1] . Worldwide, the average prevalence of SLE is 20-70 per 100.000 individuals annually. The annual incidence of SLE is 10 per 100.000 individuals [2] . The clinical manifestation of this disease varies between individuals. The pathomechanism of SLE is infuenced by ethnic, genetic, environmental, and gender factors [3] . Tumor necrosis factor-α (TNF-β) is involved in pathomechanism of SLE, but this detail is still not fully understood [4] . TNF-α levels higher signifcantly in SLE and higher in active disease status than inactive [5] . TNF-α polymorphism gives sensitivity to individuals and correlates with the disease activity, organ damage, and specifc clinical manifestations [6-8] . Increased TNF-α is associated with peripheral blood mononuclear cell apoptosis [9] . The administration of mesenchymal stem cell infusion can suppress TNF in SLE patients, thereby confrming that this cytokine is the target of SLE therapy [10] . Transforming growth factor-β is a multiregulatory cytokine for the immune system. TGF-β1 plays a role as regulatory T cell homeostasis in peripheral and T lymphocyte cells [11] . Previous studies have shown a decrease in TGF-β1 in the plasma of SLE patients, due to the production defect of TGF-β1 by lymphocytes [12] . This decrease in cytokines parallels the decline in peripheral regulatory T cells [13] . However, other studies have found no changes in TGF-β1 levels [14,15] . Heat shock protein (Hsp) is a high conserved protein expressed in physiological conditions at low levels. The levels will increase due to the response to stress stimulus [16] . Hsp70 plays a role in inhibiting apoptosis due to stress through various mechanisms. Hsp70 prevents the release of Bax, which is necessary for the